糖皮质激素及TNF-α对人角质形成细胞GRα/GRβ、NF-κB/IκB表达的影响
|
摘要
背景
糖皮质激素外用制剂是治疗炎症性皮肤病的主要药物。炎症性皮肤病患者使用糖皮质激素外用制剂易出现快速减敏和治疗抵抗等现象。然而,这些现象的确切机理尚不清楚。
糖皮质激素(GC)通过与细胞内的糖皮质激素受体(GR)结合而发挥作用。它们结合后形成二聚体结构并转位进入细胞核,进而发挥转录因子的作用。人类GR分为两种亚型:GRα和GRβ,它们起源于GR前转录物的选择性剪切。共转染检测表明GRβ通过涉及GRα/GRβ异二聚体形成的机制而具有GRα介导转录激活的显性负相抑制子的功能。这些异二聚体的形成可能解释细胞中高表达GRβ导致的激素作用效应降低的现象。GRβ对GRα活性抑制作用产生了这样一种假说:多种炎症性疾病中GRβ相对于GRα的过度表达可能扮演着细胞对激素敏感性调控的作用。
GR和核因子-κB (NF-κB)是免疫及炎症反应中两个重要的调节因素,但它们却起着完全相反的调节作用。NF-κB可介导多种与免疫和炎症相关的细胞因子和介质的活化过程,而GR则可抑制NF-κB活化基因的表达。此外,肿瘤坏死因子-α(TNF-α)也是重要的炎性细胞因子,通过激活它们的细胞内信号通路,积极参与皮肤炎症的病理生理过程。
我们的前期研究曾发现慢性皮炎表皮中GRα表达下调。然而,迄今为止,对于角质形成细胞而言,糖皮质激素对其GR和NF-κB/IκB的调节作用尚不明确。TNF-α在多种炎症性皮肤病皮损局部表达增高,在人角质形成细胞中,它对GR的表达和对NF-κB/IκB的调节作用也不清楚。皮损局部表皮GR和NF-κB/IκB的调节变化是否与外用糖皮质激素所出现的快速减敏和治疗抵抗现象有关也值得进一步探索。
目的
探讨糖皮质激素对角质形成细胞的糖皮质激素受体(GRα和GRβ)的表达、NF-κB活性及IκBα表达的调节作用;比较三种不同的糖皮质激素(氢化可的松、地塞米松、倍他米松)对角质形成细胞的糖皮质激素受体和NF-κB/IκBα调节效应的差异;探讨TNF-α对角质形成细胞的糖皮质激素受体(GRα和GRβ)表达、NF-κB活性及IκBα表达的调节作用。旨在深入理解糖皮质激素和TNF-α对角质形成细胞GRα/GRβ、NF-κB/IκBα的调节作用,为正确使用糖皮质激素外用制剂治疗炎症性皮肤病提供理论和实验依据,对阐明糖皮质激素外用制剂易出现快速减敏和治疗抵抗现象的内在机制具有积极意义。
方法与结果
1、应用SP法免疫组化技术检测慢性皮炎(慢性湿疹和慢性单纯性苔藓)与正常对照皮肤中GRα的的表达情况。结果表明,与正常对照皮肤相比,慢性皮炎中GRα的表达显著下调。
2、采用反转录Real-Time PCR和Western blotting,观察经不同浓度及不同时间的地塞米松作用下,培养的人角质形成细胞HaCaT细胞的GRα、GRβ、IκB-αmRNA和蛋白质的表达;用Western blotting法检测NF-κB核蛋白的表达情况。结果显示,地塞米松对HaCaT细胞GRα与CRβ的表达有不同的调节作用。地塞米松可下调HaCaT细胞GRα的表达,呈作用时间依赖性效应。同时,地塞米松可上调HaCaT细胞GRβ的表达,呈作用浓度依赖性效应和时间依赖性效应。地塞米松可诱导HaCaT细胞IκBα的表达而抑制NF-κB核转位,此作用呈浓度依赖性效应,在36h作用最明显。
3、将培养的人角质形成细胞HaCaT细胞分为空白对照组、氢化可的松作用组、地塞米松作用组、倍他米松作用组,采用反转录Real-Time PCR和Western blotting法检测各组HaCaT细胞的GRα、GRβ、IκBαmRNA和蛋白质表达,用Western blotting法检测NF-κB核蛋白的表达情况。结果显示,三种激素均具有下调HaCaT细胞GRα表达的作用,其中氢化可的松作用最弱,而地塞米松与倍他米松作用之间无明显差异;三种激素均具有上调HaCaT细胞GRβ表达的作用,但此作用之间无明显差异。三种激素均具有诱导HaCaT细胞IκBα的表达而抑制NF-κB核转位的作用,其中氢化可的松作用最弱,而地塞米松与倍他米松作用之间无明显差异。
4、采用反转录Real-Time PCR和Western blotting,观察经不同浓度及不同时间的肿瘤坏死因子(TNF-α)作用下,培养的人角质形成细胞HaCaT细胞的GRα、GRβ、IκBαmRNA和蛋白质表达,用Western blotting法检测NF-κB核蛋白的表达情况。结果显示,TNF-α对HaCaT细胞GRα的表达无明显影响,但可上调HaCaT细胞GRβ的表达,并且呈剂量和时间依赖性的上调趋势。TNF-α可抑制HaCaT细胞IκBα的表达而诱导NF-κB的核转位,呈作用浓度依赖性效应,此作用在1h达到高峰,此后逐渐减弱。
结论
1、与正常对照皮肤相比,慢性皮炎中GRα表达的下调可能会干扰皮损局部的抗炎机制并限制外用激素的疗效。
2、糖皮质激素对角质形成细胞GRα和GRβ表达的不同调节作用可能部分解释外用糖皮质激素制剂的皮肤耐受现象和对糖皮质激素的抵抗。糖皮质激素通过调控人角质形成细胞NF-κB/IκB信号通路,可抑制皮损局部的炎症反应。
3、不同效力的糖皮质激素对角质形成细胞GRα和GRβ的调节效力不同,对角质形成细胞NF-κB/IκB的调节效力也不同。这提示了临床上正确选用不同效力糖皮质激素外用制剂的必要性。
4、TNF-α不但可通过调控角质形成细胞NF-κB/IκB可参与皮肤的炎症反应,而且还可诱导角质形成细胞GRβ的过度表达。后者可能是炎性细胞因子参与诱发糖皮质激素皮肤耐受现象的内在机制之一。
Background
Topical glucocorticoid therapy is mainly a routine therapeutic modality for the treatment of inflammatory skin deseases. Tachyphylaxis and resistance to topical glucocorticoid agents often occur during the treatment of inflammatory skin deseases. However, the mechanisms of tachyphylaxis and resistance to topical glucocorticoid therapy are unknown.
Glucocorticoids work by binding to the cytosolic glucocorticoid receptor (GR), inducing the formation of a dimer that is translocated into the nucleus and acts as a transcription factor. Cloning of the human GR has identified two isoforms, termed GRαand GRβ, which originate from alternative splicing of the GR primary transcript. Co-transfection assays have shown GRβto function as a dominant-negative inhibitor of GRα–mediated transcriptional activation through a mechanism that involves the formation of GRα/GRβheterodimers. Such heterodimer formation may account for the reduced effectiveness of glucocorticoid action in cells overexpressing GRβ. This inhibitory effect of GRβon GRαactivity led to the hypothesis that excessive expression of the GRβisoform with respect to GRαmight play a role in the regulation of a cell’s sensitivity to glucocorticoids in various inflammatory diseases.
GR and nuclear factorκB (NF-κB) are both important regulatory factors, with entirely opposite effects, involved in immune response and inflammation. NF-κB plays a role in activating transcription of many cytokines and mediators associated with immune response or inflammation while GR may inhibit gene expression of many cytokines and mediators activated by NF-κB. Moreover, TNF-αis important inflammatory cytokines actively participating in pathophysiological process of skin inflammation via activating their intracellular signaling pathway.
Our previous studies has shown the downregulated expression of GRαin chronic dermatitis. However, effects of glucocorticoid on expression of glucocorticoid receptor and NF-κB/IκB in human keratinocytes remain unknown up till now. Effects of overexpressing
TNF-αin local skin of inflammatory skin deseases on expression of glucocorticoid receptor and NF-κB/IκB in human keratinocytes are unclear also. Whether do they associated with phenomenon of tachyphylaxis and resistance to topical glucocorticoid therapy in inflammatory skin deseases?
Objective
To reconfirm expression of GRαin chronic dermatitides.
To investigate Effects of dexamethasone on expression of glucocorticoid receptor and regulation of NF-κB/IκB in human keratinocyte HaCaT cell line, to compare differences in effects of different glucocorticoids on expression of glucocorticoid receptor and regulation of NF-κB/IκB in human keratinocyte HaCaT cell line, and to investigate effects of TNF-αon expression of glucocorticoid receptor and regulation of NF-κB/IκB in human keratinocyte HaCaT cell line, for further insights into the mechanism of tachyphylaxis and resistance to topical glucocorticoid therapy.
Methods and Results
1. The expressions of GRαin chronic dermatitides (chronic eczema and lichen simplex chronicus) and control normal skin specimens were analyzed using Streptavidin peroxidase (SP) immunohistochemical technique. Immunohistochemistry analysis reconfirmed that expression of GRαwas down-regulated in chronic dermatitides compared with control normal skin.
2. Cultured HaCaT cells were treated by dexamethasone with different concentrations and for different durations. The expressions of GRα,βand IκB-αmRNA and protein were examined by Reverse transcription-Real time polymerase chain reaction (RT-PCR) and Western blotting. The expressions of NF-κB neucleoprotein were examined by Western blotting. Dexamethasone could down-regulate the expression of GRαin HaCaT cells in a time-dependent manner, while dexamethasone could up-regulatewith the expression of GRβin HaCaT cells in a time- and dose-dependent manner. Dexamethasone could up-regulate the expression of IκB-αmeanwhile down-regulate with the expression of NF-κB neucleoprotein in HaCaT cells in a dose-dependent manner. The effects were most obvious with treatment of dexamethasone for 36 h.
3. Cultured HaCaT cells were divided into hydrocortisone stimulation group and dexamethasone stimulation group and betamethasone stimulation group. The expressions of GRα,βand IκBαmRNA and protein were examined by Reverse transcription-Real time polymerase chain reaction (RT-PCR) and Western blotting. The expressions of NF-κB neucleoprotein were examined by Western blotting. The three kinds of the glucocorticoids with different efficacy could down-regulate the expression of GRαin HaCaT cells, hydrocortisone had most poorly effect while no difference between dexamethasone with betamethasone exists. The three kinds of glucocorticoid could up-regulate the expression of GRβin HaCaT cells,but no difference exists among them. These glucocorticoid could up-regulate the expression of IκBαmeanwhile down-regulate the expression of NF-κB neucleoprotein in HaCaT cells, hydrocortisone had most poorly effect whil no difference between dexamethasone with betamethasone.
4. Cultured HaCaT cells were treated by TNF-αwith different concentrations and for different durations. The expressions of GRα,βand IκBαmRNA and protein were examined by Reverse transcription-Real time polymerase chain reaction (RT-PCR) and Western blotting. The expressions of NF-κB neucleoprotein were examined by Western blotting. TNF-αhad no effects on expression of GRαin HaCaT cells, but up-regulate the expression of GRβin HaCaT cells in a time- and dose-dependent manner. TNF-αcould down-regulate the expression of IκBαmeanwhile up-regulate the expression of NF-κB neucleoprotein in HaCaT cells in a dose-dependent manner. The effects were most obvious with treatment of TNF-αfor 1h then went down.
Conclusion
1. Decreased expression of GRαin chronic dermatitides might interfere with anti-inflammation mechanism in cutaneous lesions and limit therapeutic effect of topical glucocorticoid agents.
2. The different regulations on the expression of GRαand GRβin keratinocytes by GC may partly explain the tachyphylaxis and resistance to topical glucocorticoid therapy. Glucocorticoid might suppresse inflammatory reaction by affecting NF-κB/IκB in skin lesions.
3. The different effects on the expression of GRαand GRβin keratinocytes by different GC could give guidance for correctly using glucocorticoids with different efficacy. The different effects on the NF-κB/IκB in keratinocytes by different GCs could be helpful to control different inflammatory situations in dermatitides.
4. TNF-αcan increase the expression of GRβ, which may be one of the mechanisms of glucocorticoid resistance induced by inflammatory cytokines. TNF-αmight participates in inflammatory process via regulating NF-κB/IκB in keratinocytes.
糖皮质激素外用制剂是治疗炎症性皮肤病的主要药物。炎症性皮肤病患者使用糖皮质激素外用制剂易出现快速减敏和治疗抵抗等现象。然而,这些现象的确切机理尚不清楚。
糖皮质激素(GC)通过与细胞内的糖皮质激素受体(GR)结合而发挥作用。它们结合后形成二聚体结构并转位进入细胞核,进而发挥转录因子的作用。人类GR分为两种亚型:GRα和GRβ,它们起源于GR前转录物的选择性剪切。共转染检测表明GRβ通过涉及GRα/GRβ异二聚体形成的机制而具有GRα介导转录激活的显性负相抑制子的功能。这些异二聚体的形成可能解释细胞中高表达GRβ导致的激素作用效应降低的现象。GRβ对GRα活性抑制作用产生了这样一种假说:多种炎症性疾病中GRβ相对于GRα的过度表达可能扮演着细胞对激素敏感性调控的作用。
GR和核因子-κB (NF-κB)是免疫及炎症反应中两个重要的调节因素,但它们却起着完全相反的调节作用。NF-κB可介导多种与免疫和炎症相关的细胞因子和介质的活化过程,而GR则可抑制NF-κB活化基因的表达。此外,肿瘤坏死因子-α(TNF-α)也是重要的炎性细胞因子,通过激活它们的细胞内信号通路,积极参与皮肤炎症的病理生理过程。
我们的前期研究曾发现慢性皮炎表皮中GRα表达下调。然而,迄今为止,对于角质形成细胞而言,糖皮质激素对其GR和NF-κB/IκB的调节作用尚不明确。TNF-α在多种炎症性皮肤病皮损局部表达增高,在人角质形成细胞中,它对GR的表达和对NF-κB/IκB的调节作用也不清楚。皮损局部表皮GR和NF-κB/IκB的调节变化是否与外用糖皮质激素所出现的快速减敏和治疗抵抗现象有关也值得进一步探索。
目的
探讨糖皮质激素对角质形成细胞的糖皮质激素受体(GRα和GRβ)的表达、NF-κB活性及IκBα表达的调节作用;比较三种不同的糖皮质激素(氢化可的松、地塞米松、倍他米松)对角质形成细胞的糖皮质激素受体和NF-κB/IκBα调节效应的差异;探讨TNF-α对角质形成细胞的糖皮质激素受体(GRα和GRβ)表达、NF-κB活性及IκBα表达的调节作用。旨在深入理解糖皮质激素和TNF-α对角质形成细胞GRα/GRβ、NF-κB/IκBα的调节作用,为正确使用糖皮质激素外用制剂治疗炎症性皮肤病提供理论和实验依据,对阐明糖皮质激素外用制剂易出现快速减敏和治疗抵抗现象的内在机制具有积极意义。
方法与结果
1、应用SP法免疫组化技术检测慢性皮炎(慢性湿疹和慢性单纯性苔藓)与正常对照皮肤中GRα的的表达情况。结果表明,与正常对照皮肤相比,慢性皮炎中GRα的表达显著下调。
2、采用反转录Real-Time PCR和Western blotting,观察经不同浓度及不同时间的地塞米松作用下,培养的人角质形成细胞HaCaT细胞的GRα、GRβ、IκB-αmRNA和蛋白质的表达;用Western blotting法检测NF-κB核蛋白的表达情况。结果显示,地塞米松对HaCaT细胞GRα与CRβ的表达有不同的调节作用。地塞米松可下调HaCaT细胞GRα的表达,呈作用时间依赖性效应。同时,地塞米松可上调HaCaT细胞GRβ的表达,呈作用浓度依赖性效应和时间依赖性效应。地塞米松可诱导HaCaT细胞IκBα的表达而抑制NF-κB核转位,此作用呈浓度依赖性效应,在36h作用最明显。
3、将培养的人角质形成细胞HaCaT细胞分为空白对照组、氢化可的松作用组、地塞米松作用组、倍他米松作用组,采用反转录Real-Time PCR和Western blotting法检测各组HaCaT细胞的GRα、GRβ、IκBαmRNA和蛋白质表达,用Western blotting法检测NF-κB核蛋白的表达情况。结果显示,三种激素均具有下调HaCaT细胞GRα表达的作用,其中氢化可的松作用最弱,而地塞米松与倍他米松作用之间无明显差异;三种激素均具有上调HaCaT细胞GRβ表达的作用,但此作用之间无明显差异。三种激素均具有诱导HaCaT细胞IκBα的表达而抑制NF-κB核转位的作用,其中氢化可的松作用最弱,而地塞米松与倍他米松作用之间无明显差异。
4、采用反转录Real-Time PCR和Western blotting,观察经不同浓度及不同时间的肿瘤坏死因子(TNF-α)作用下,培养的人角质形成细胞HaCaT细胞的GRα、GRβ、IκBαmRNA和蛋白质表达,用Western blotting法检测NF-κB核蛋白的表达情况。结果显示,TNF-α对HaCaT细胞GRα的表达无明显影响,但可上调HaCaT细胞GRβ的表达,并且呈剂量和时间依赖性的上调趋势。TNF-α可抑制HaCaT细胞IκBα的表达而诱导NF-κB的核转位,呈作用浓度依赖性效应,此作用在1h达到高峰,此后逐渐减弱。
结论
1、与正常对照皮肤相比,慢性皮炎中GRα表达的下调可能会干扰皮损局部的抗炎机制并限制外用激素的疗效。
2、糖皮质激素对角质形成细胞GRα和GRβ表达的不同调节作用可能部分解释外用糖皮质激素制剂的皮肤耐受现象和对糖皮质激素的抵抗。糖皮质激素通过调控人角质形成细胞NF-κB/IκB信号通路,可抑制皮损局部的炎症反应。
3、不同效力的糖皮质激素对角质形成细胞GRα和GRβ的调节效力不同,对角质形成细胞NF-κB/IκB的调节效力也不同。这提示了临床上正确选用不同效力糖皮质激素外用制剂的必要性。
4、TNF-α不但可通过调控角质形成细胞NF-κB/IκB可参与皮肤的炎症反应,而且还可诱导角质形成细胞GRβ的过度表达。后者可能是炎性细胞因子参与诱发糖皮质激素皮肤耐受现象的内在机制之一。
Background
Topical glucocorticoid therapy is mainly a routine therapeutic modality for the treatment of inflammatory skin deseases. Tachyphylaxis and resistance to topical glucocorticoid agents often occur during the treatment of inflammatory skin deseases. However, the mechanisms of tachyphylaxis and resistance to topical glucocorticoid therapy are unknown.
Glucocorticoids work by binding to the cytosolic glucocorticoid receptor (GR), inducing the formation of a dimer that is translocated into the nucleus and acts as a transcription factor. Cloning of the human GR has identified two isoforms, termed GRαand GRβ, which originate from alternative splicing of the GR primary transcript. Co-transfection assays have shown GRβto function as a dominant-negative inhibitor of GRα–mediated transcriptional activation through a mechanism that involves the formation of GRα/GRβheterodimers. Such heterodimer formation may account for the reduced effectiveness of glucocorticoid action in cells overexpressing GRβ. This inhibitory effect of GRβon GRαactivity led to the hypothesis that excessive expression of the GRβisoform with respect to GRαmight play a role in the regulation of a cell’s sensitivity to glucocorticoids in various inflammatory diseases.
GR and nuclear factorκB (NF-κB) are both important regulatory factors, with entirely opposite effects, involved in immune response and inflammation. NF-κB plays a role in activating transcription of many cytokines and mediators associated with immune response or inflammation while GR may inhibit gene expression of many cytokines and mediators activated by NF-κB. Moreover, TNF-αis important inflammatory cytokines actively participating in pathophysiological process of skin inflammation via activating their intracellular signaling pathway.
Our previous studies has shown the downregulated expression of GRαin chronic dermatitis. However, effects of glucocorticoid on expression of glucocorticoid receptor and NF-κB/IκB in human keratinocytes remain unknown up till now. Effects of overexpressing
TNF-αin local skin of inflammatory skin deseases on expression of glucocorticoid receptor and NF-κB/IκB in human keratinocytes are unclear also. Whether do they associated with phenomenon of tachyphylaxis and resistance to topical glucocorticoid therapy in inflammatory skin deseases?
Objective
To reconfirm expression of GRαin chronic dermatitides.
To investigate Effects of dexamethasone on expression of glucocorticoid receptor and regulation of NF-κB/IκB in human keratinocyte HaCaT cell line, to compare differences in effects of different glucocorticoids on expression of glucocorticoid receptor and regulation of NF-κB/IκB in human keratinocyte HaCaT cell line, and to investigate effects of TNF-αon expression of glucocorticoid receptor and regulation of NF-κB/IκB in human keratinocyte HaCaT cell line, for further insights into the mechanism of tachyphylaxis and resistance to topical glucocorticoid therapy.
Methods and Results
1. The expressions of GRαin chronic dermatitides (chronic eczema and lichen simplex chronicus) and control normal skin specimens were analyzed using Streptavidin peroxidase (SP) immunohistochemical technique. Immunohistochemistry analysis reconfirmed that expression of GRαwas down-regulated in chronic dermatitides compared with control normal skin.
2. Cultured HaCaT cells were treated by dexamethasone with different concentrations and for different durations. The expressions of GRα,βand IκB-αmRNA and protein were examined by Reverse transcription-Real time polymerase chain reaction (RT-PCR) and Western blotting. The expressions of NF-κB neucleoprotein were examined by Western blotting. Dexamethasone could down-regulate the expression of GRαin HaCaT cells in a time-dependent manner, while dexamethasone could up-regulatewith the expression of GRβin HaCaT cells in a time- and dose-dependent manner. Dexamethasone could up-regulate the expression of IκB-αmeanwhile down-regulate with the expression of NF-κB neucleoprotein in HaCaT cells in a dose-dependent manner. The effects were most obvious with treatment of dexamethasone for 36 h.
3. Cultured HaCaT cells were divided into hydrocortisone stimulation group and dexamethasone stimulation group and betamethasone stimulation group. The expressions of GRα,βand IκBαmRNA and protein were examined by Reverse transcription-Real time polymerase chain reaction (RT-PCR) and Western blotting. The expressions of NF-κB neucleoprotein were examined by Western blotting. The three kinds of the glucocorticoids with different efficacy could down-regulate the expression of GRαin HaCaT cells, hydrocortisone had most poorly effect while no difference between dexamethasone with betamethasone exists. The three kinds of glucocorticoid could up-regulate the expression of GRβin HaCaT cells,but no difference exists among them. These glucocorticoid could up-regulate the expression of IκBαmeanwhile down-regulate the expression of NF-κB neucleoprotein in HaCaT cells, hydrocortisone had most poorly effect whil no difference between dexamethasone with betamethasone.
4. Cultured HaCaT cells were treated by TNF-αwith different concentrations and for different durations. The expressions of GRα,βand IκBαmRNA and protein were examined by Reverse transcription-Real time polymerase chain reaction (RT-PCR) and Western blotting. The expressions of NF-κB neucleoprotein were examined by Western blotting. TNF-αhad no effects on expression of GRαin HaCaT cells, but up-regulate the expression of GRβin HaCaT cells in a time- and dose-dependent manner. TNF-αcould down-regulate the expression of IκBαmeanwhile up-regulate the expression of NF-κB neucleoprotein in HaCaT cells in a dose-dependent manner. The effects were most obvious with treatment of TNF-αfor 1h then went down.
Conclusion
1. Decreased expression of GRαin chronic dermatitides might interfere with anti-inflammation mechanism in cutaneous lesions and limit therapeutic effect of topical glucocorticoid agents.
2. The different regulations on the expression of GRαand GRβin keratinocytes by GC may partly explain the tachyphylaxis and resistance to topical glucocorticoid therapy. Glucocorticoid might suppresse inflammatory reaction by affecting NF-κB/IκB in skin lesions.
3. The different effects on the expression of GRαand GRβin keratinocytes by different GC could give guidance for correctly using glucocorticoids with different efficacy. The different effects on the NF-κB/IκB in keratinocytes by different GCs could be helpful to control different inflammatory situations in dermatitides.
4. TNF-αcan increase the expression of GRβ, which may be one of the mechanisms of glucocorticoid resistance induced by inflammatory cytokines. TNF-αmight participates in inflammatory process via regulating NF-κB/IκB in keratinocytes.
引文
1. Pace TW, Hu F, Miller AH. Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. Brain Behav Immun. 2007; 21(1): 9-19.
2. Duma D, Jewell CM, Cidlowski JA. Multiple glucocorticoid receptor isoforms and mechanisms of post-translational modification. J Steroid BiochemMol Biol. 2006; 102(1-5): 11-21.
3. Schaaf MJ, Cidlowski A. Molecular mechanisms of glucocorticoid action and resistance. J Steroid BiochemMol Biol. 2003; 83(1): 37-48.
4. Cho YJ, Lee KE. Decreased glucocorticoid binding affinity to glucocorticoid receptor is important in the poor response to steroid therapy of older-aged patients with severe bronchial asthma. Allergy Asthma Proc. 2003, 24(5): 353-358.
5. Pujols L, Xaubet A, Ramirez J, et al. Expression of glucocorticoid receptors alpha and beta in steroid sensitive and steroid insensitive interstitial lung diseases. Thorax. 2004; 59(8): 687-693.
6. Raddatz D, Middel P, Bockemuhl M. Glucocorticoid receptor expression in inflammatory bowel disease: evidence for a mucosal down-regulation in steroid-unresponsive ulcerative colitis. Aliment Pharmacol Ther. 2004; 19(1): 47-61.
7. Yudt MR, Jewell CM, Bienstock RJ, et al. Molecular origins for the dominant negative function of human glucocorticoid receptor beta. Mol Cell Biol. 2003; 23(12): 4319-4330.
8. Pujols L, Mullol J, Picado C. Alpha and beta glucocorticoid receptors: relevance in airway diseases. Curr Allergy Asthma Rep. 2007; 7(2): 93-99.
9. Lewis-Tuffin LJ, Cidlowski JA. The physiology of human glucocorticoid receptor beta (hGRbeta) and glucocorticoid resistance. Ann N Y Acad Sci. 2006; 1069(6): 1-9.
10. Lu N, Cidlowski J. The origin and functions of multiple human glucocorticoid receptor isoforms. Ann N Y Acad Sci. 2004; 1024 (6): 102-123.
11.杨玲,何威,黎智,等。糖皮质激素受体α、核因子-κB、肿瘤坏死因子-α和白介素-1β在慢性皮炎中的表达.临床皮肤科杂志, 2006, 35(5): 291-293.
12. Ghosh S, Karin M. Missing pieces in the NF-κB puzzle. Cell. 2002; 109(Suppl): s81-s96.
13. Li Q, Verma IM. NF-κB regulation in the immune system. Nat Rev Immunol. 2002; 2 (10): 725-734.
14. Qin JZ, Chaturvedi V, Denning MF, et al. Role of NF-κB in the apoptotic-resistant phenotype of keratinocyte. J Biol Chem. 1999; 274(53): 37957-37964.
15. Seitz CS, Freiberg RA, Hinata K, et al. NF-κB determines localization and features of cell death in epidermis. J Clin Invest. 2000; 105(3): 253-260.
16. Auphan N, DiDonato JA, Rosette C, et al. Immunosuppression by glucocorticoids: inhibition of NF-κB activity through induction of IκB synthesis. Science. 1995; 270 (5234): 286-290.
17. Westergaard M, Henningsen J, Johansen C, et al. Expression and localization of peroxisome proliferators-activated receptors and nuclear factor-kappaB in BoFmal and lesional psoriatic skin. J Invest Dermatol. 2003; 121(5): 1104-1117.
18. Monici MC, Agu ennouz M, Mazzeo A, et al. Activation of nuclear factor-kappaB in inflammatory,myopathies and Duchenne muscular dystrophy. Neurology. 2003; 60(6): 993-997.
19.宋艳丽,文海泉,肖嵘,等.卡介苗多糖核酸调节特应性皮炎患者PBMC中NF-kB和Th1/Th2细胞因子的表达.中华皮肤科杂志. 2007; 40(1): 42-44.
20. Rhodus NL, Cheng B, Myers S, et al. The feasibility of monitoring NF-kappaB associated cytokines: TNF-alpha, IL-1alpha, IL-6, and IL-8 in whole saliva for the malignant transformation of oral lichen planus. Mol Carcinog. 2005; 44(2): 77-82.
21. Rhodus NL, Cheng B, Bowles W, et al. Proinflammatory cytokine levels in saliva before and after treatment of (erosive) oral lichen planus with dexamethasone. Oral Dis. 2006; 12(2): 112-116.
22. Murphy JE, Rebort C, Kupper TS. Interleukin-1 and cutaneous inflammation: a crucial ling between innate and acquired immunity. J Invest Dermatol. 2000; 114(3): 602-608.
23. Robort C, Kupper TS. Inflammatory skin diseases, T cell, and immunsurveillance. N Engl J Med. 1999; 341(24): 1817-1828.
24.冯信忠,陆毅, Corrine L, et al.细胞因子在银屑病非皮损成纤维细胞中的表达.中华皮肤科杂志. 2003; 36 (3): 133-135.
25.王万卷,陈丽,王晓鹏.寻常型银屑病皮损中肿瘤坏死因子-α、基质金属蛋白酶9及其抑制剂-1的表达.西安交通大学学报(医学版). 2007; 28(3): 322-324.
26. Groves RW, Allen MH, Ross EL, et al. Tumor necrosis factor alpha is pro-inflammtary in normal human skin and modulates cutaneous adhesion molecule expression. Br J Dermatol. 1995; 132(3): 345-352.
27. Sheu MY, Fowler AJ, Kao J, et al. Topical peroxisome proliferators activated receptor-alpha activators reduce inflammation in irritant and allergic contant dermatitis models. J Invest Dermatol. 2002; 118(1): 94-101.
28. Kino T, Chrousos GP. Tumor necrosis factor alpha receptor- and Fas-associated FLASH inhibit transcriptional activity of the glucocorticoid receptor by binding to and interfering with its interaction with p160 type nuclear receptor coactivators. J Biol Chem. 2003; 278(5): 3023-3029.
29. Webster JC, Oakley RH, Jewell CM, et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance. Proc Natl Acad Sci. 2001; 98(12): 6865-6870.
1.陈锡唐,等.实用皮肤组织病理学.广州:广东科技出版社. 1994: 163-168.
2.杨玲,何威,黎智,等.糖皮质激素受体α、核因子-κB、肿瘤坏死因子-α和白介素-1β在慢性皮炎中的表达.临床皮肤科杂志. 2006; 35(5): 291-293.
3.王志红,肖素芳,林海,等.烫伤大鼠糖皮质激素受体减少与全身炎症反应综合征的关系.福建医科大学学报. 2000; 34(1): 39-40.
4. Cidlowski JA, Cidlowski NB. Regulation of glucocorticoid receptors by glucocorticoids in cultured HeLa S3 cells. Endocrinology. 1981; 109(6): 1975-1982.
5. Svec F, Rudis M. Glucocorticoids regulate the glucocorticoid receptor in the AtT20 cell. J Biol Chem. 1981; 256(12): 5984-5987.
6. Danielsen M, Stallcup M. Down-regulation of the glucocorticoid receptor in mouse lymphoma cell variants. Mol Cell Biol. 1984; 4(3): 449-453.
7. Silva C, Powell-Oliver F, Cidlowski J. Regulation of the human glucocorticoid receptor by long-term and chronic treatment with glucocorticoids. Steroids. 1994; 59(7): 436-442.
8. Dong Y, Poellinger L, Gustafsson J, et al. Regulation of the glucocorticoid receptor expression: Evidence for transcriptional and posttranslational mechanisms. Mol Endocrin. 1988; 2(12): 1256-1264.
9. Burnstein K, Jewell C, Cidlowski J. Human glucocorticoid receptor cDNA contains sequences sufficient for receptor down-regulation. J Biol Chem. 1990; 265(13): 7284-7291.
10. Burnstein K, Bellingham D, Jewell C, et al. Autoregulation of glucocorticoid receptor gene expression. Steroids. 1991; 56(2): 52-58.
11. Bellingham D, Sar M, Cidlowski J. Ligand-dependent downregulation of stably transfected glucocorticoid receptors is associated with the loss of functional glucocorticoid responsiveness. Mol Endocrinol. 1992; 6(12): 2090-2102.
12. Hoeck W, Rusconi S, Groner B. Down-regulation and phosphorylation of the glucocorticoid receptors in cultured cells. Investigations with a monospecific antiserumagainst a bacterially expressed receptor fragment. J Biol Chem. 1989; 264(24): 14396-14402.
13. Vachier I, Chiappara G, Vignola AM, et al. Glucocorticoid receptors in bronchial epithelial cells in asthma. Am J Respir Crit Care Med. 1998; 158(3): 963-970.
14. Karl M, Lamberts SW, Detera-Wadleigh SD, et al. Familial glucocorticoid resistance caused by a splice site deletion in the human glucocorticoid receptor gene. J Clin Endocrinol Metab. 1993; 76(3): 683-689.
15. Adcock IM. Steroid resistance in asthma. Molecular mechanisms.Am J Respir Crit Care Med. 1996; 154(2 Pt 2): S58–61.
1.杨玲,何威,黎智,等.糖皮质激素受体α、核因子-κB、肿瘤坏死因子-α和白介素-1β在慢性皮炎中的表达.临床皮肤科杂志. 2006; 35(5): 291-293.
2. Xu M, Song L, Wang Z. Effects of Dexamethasone on glucocorticoid receptor expression in a human ovarian carcinoma cell line 3AO. Chin Med J (Engl). 2003; 116(3): 392-395.
3.李波,白祥军,王海平.地塞米松对人单核细胞糖皮质激素受体蛋白表达的影响.中华急诊医学杂志. 2006; 15(6): 525-528.
4. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and 2 (-Delta Delta C (T). Methods. Methods, 2001; 25(4): 402-408.
5. Pace TW, Hu F, Miller AH. Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. Brain Behav Immun. 2007; 21(1): 9-19.
6. Duma D, Jewell CM, Cidlowski JA. Multiple glucocorticoid receptor isoforms and mechanisms of post-translational modification. J Steroid BiochemMol Biol. 2006; 102(1-5): 11-21.
7. Schaaf MJ, Cidlowski A. Molecular mechanisms of glucocorticoid action and resistance. J Steroid BiochemMol Biol. 2003; 83(1):37-48.
8. Albrecht M, Janssen M, Konrad L, et al. Effects of dexamethasone on proliferation of and fibronectin synthesis by human primary prostatic stromal cells in vitro. Andrologia. 2002; 34(1): 11-21.
9. Cho YJ, Lee KE. Decreased glucocorticoid binding affinity to glucocorticoid receptor is important in the poor response to steroid therapy of older-aged patients with severe bronchial asthma. Allergy Asthma Proc. 2003; 24(5): 353-358.
10. Pujols L, Xaubet A, Ramirez J, et al. Expression of glucocorticoid receptors alpha and beta in steroid sensitive and steroid insensitive interstitial lung diseases. Thorax. 2004; 59(8): 687-693.
11. Raddatz D, Middel P, Bockemuhl M. Glucocorticoid receptor expression in inflammatory bowel disease: evidence for a mucosal down-regulation in steroid-unresponsive ulcerative colitis. Aliment Pharmacol Ther. 2004; 19(1): 47-61.
12. Yudt MR, Jewell CM, Bienstock RJ, et al. Molecular origins for the dominant negative function of human glucocorticoid receptor beta. Mol Cell Biol. 2003; 23(12): 4319-4330.
13. Pujols L, Mullol J, Picado C. Alpha and beta glucocorticoid receptors: relevance in airway diseases. Curr Allergy Asthma Rep. 2007; 7(2): 93-99.
14. Lewis-Tuffin LJ, Cidlowski JA. The physiology of human glucocorticoid receptor beta ( hGRbeta ) and glucocorticoid resistance. Ann N Y Acad Sci. 2006; 1069(6): 1-9.
15. Webster JC, Oakley RH, Jewell CM, et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance. Proc Natl Acad Sci. 2001; 98(12): 6865-6870.
16. Lu N, Cidlowski J. The origin and functions of multiple human glucocorticoid receptor isoforms. Ann N Y Acad Sci. 2004; 1024 (6): 102-123.
1. Minguet S, Huber M, Rosenkranz L. Adenosine and cAMP are potent inhibitors of the NF-kappa B pathway downstream of immunoreceptors. Eur J Immunol. 2005; 35(1): 31-41.
2. Zhang Q, Li PH. Research advances on relationship between nudear factor-kB and glaucoma. Int J Ophthalmo. 2006; 6(4): 840-843.
3. Gavrilyuk V, Dello Russo C, Heneka MT, et al. Norepinephrine increases I kappa B alpha expression in astrocytes. J Biol Chem. 2002; 277(33): 29662-29668.
4. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and 2-Delta Delta C (T). Methods. Methods. 2001; 25(4): 402-408.
5. Mori NF, Shirakawa H, Shimizu S, et al. Transcriptional regulation of the human interleukin-6 gene promoter in human T cell leukem ia virus typeéinfected T cell lines: evidence for the involvement of NF-кB. Blood. 1994; 84(9): 2904-2914.
6. Ghosh S, Karin M. Missing pieces in the NF-κB puzzle. Cell, 2002; 109(Suppl): s81-s96.
7. Li Q, Verma IM. NF-κB regulation in the immune system. Nat Rev Immunol. 2002; 2 (10): 725-734.
8. Qin JZ, Chaturvedi V, Denning MF, et al. Role of NF-κB in the apoptotic-resistant phenotype of keratinocyte. J Biol Chem. 1999; 274(53): 37957-37964.
9. Seitz CS, Freiberg RA, Hinata K, et al. NF-κB determines localization and features of cell death in epidermis. J Clin Invest. 2000; 105(3): 253-260.
10. Auphan N, DiDonato JA, Rosette C, et al. Immunosuppression by glucocorticoids: inhibition of NF-κB activity through induction of IκB synthesis. Science. 1995; 270 (5234): 286-290.
11. Westergaard M, Henningsen J, Johansen C, et al. Expression and localization of peroxisome proliferators-activated receptors and nuclear factor-kappaB in BoFmal and lesional psoriatic skin. J Invest Dermatol. 2003; 121(5): 1104-1117.
12. Monici MC, Agu ennouz M, Mazzeo A, et al. Activation of nuclear factor-kappaB in inflammatory,myopathies and Duchenne muscular dystrophy. Neurology. 2003; 60(6): 993-997.
13.宋艳丽,文海泉,肖嵘,等.卡介苗多糖核酸调节特应性皮炎患者PBMC中NF-kB和Th1/Th2细胞因子的表达.中华皮肤科杂志. 2007; 40(1): 42-44.
14. Rhodus NL, Cheng B, Myers S, et al. The feasibility of monitoring NF-kappaB associated cytokines: TNF-alpha, IL-1alpha, IL-6, and IL-8 in whole saliva for the malignant transformation of oral lichen planus. Mol Carcinog. 2005; 44(2): 77-82.
15. Rhodus NL, Cheng B, Bowles W, et al. Proinflammatory cytokine levels in saliva before and after treatment of (erosive) oral lichen planus with dexamethasone. Oral Dis. 2006; 12(2): 112-116.
16. Tao Y, Williams-Skipp C, Scheinman RI. Mapping of glucocorticoid receptor DNA binding domain surfaces contributing to transrepression of NF-kappa B and induction of apoptosis. J Biol Chem. 2001; 276(4): 2329-2332.
17. Deroo BJ, Archer TK. Glucocorticoid receptor activation of the I kappa B alpha promoter within chromatin. Mol Biol Cell. 2001; 12(11): 3365-3374.
18. Brostjan C, Anrather J, Csizmadia V, et al. Glucocorticoid–mediated repression of NF-kappaB activity in endothelial cells does not involve induction of I-kappaB alpha synthesis. J Biol Chem. 1996; 271(32): 19612-19616.
1. Bray PJ, Cotton RG. Variations of the human glucocorticoid receptor gene (NR3C1): pathological and in vitro mutations and polymorphisms. Hum Mutat. 2003; 21(6): 557-568.
2. Schaaf MJ, Cidlowski A. Molecular mechanisms of glucocorticoid action and resistance. J Steroid BiochemMol Biol. 2003; 83(1): 37-48.
3. de Castro M, Elliot S, Kino T, et al. The non-ligand binding beta-isoform of the human glucocorticoid receptor (hGR beta) tissue levels, mechanism of action, and potential physiologic role. Mol Med. 1996; 2(5): 597-607.
4. Hamid QA, Wenzel SE, Hauk PJ, et al. Increased glucocorticoid receptor beta in airway cells of glucocorticoid-insensitive asthma. Am J Respir Crit Care Med. 1999; 159(5 Pt 1): 1600-1604.
5. Honda M, Orii F, Ayabe T, et al. Expression of glucocorticoid receptor beta in lymphocytes of patients with glucocorticoid-resistant ulcerative colitis. Gastroenterology. 2000; 118(5): 859-866.
6. Chikanza C. Mechanisms of glucocorticoid resistance in rheumatoid arthritis: a putative role for the corticosteroid receptor beta isoform. Ann N Y Acad Sci, 2002; 966(6): 39-48.
7.张星虎,许贤豪,殷剑,等.重症肌无力患者糖皮质激素受体检测的临床价值.中华内科杂志. 2002; 41(5): 322-324.
8. Webster JC, Oakley RH, Jewell CM, et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance. Proc Natl Acad Sci. 2001; 98(12): 6865-6870.
9.何庆南,易著文,何小解,等. GRβ在肾病综合征患儿中的表达及影响因素研究.中国病理生理杂志. 2002; 18(9): 1042-1045.
10. Oakley RH, Jewell CM, Yudt MR, et al. The dominant negative activity of the human glucocorticoid receptor beta isoform: Specificity and mechanisms of action. J Biol Chem. 1999, 274(39): 27857-27866.
11. Hauk PJ, Hamid QA, Chrousos GP, et al. Induction of corticosteroid insensitivity inhuman PBMCs by microbial superantigens. Allergy Clin Immunol. 2000; 105(4): 782-787.
12. Lu N, Cidlowski J. The origin and functions of multiple human glucocorticoid receptor isoforms. Ann N Y Acad Sci. 2004; 1024(6): 102-123.
1. Minguet S, Huber M, Rosenkranz L. Adenosine and cAMP are potent inhibitors of the NF- kappa B pathway downstream of immunoreceptors. Eur J Immunol. 2005; 35(1): 25-30.
2. Zhang Q, Li PH. Research advances on relationship between nudear factor- kB and glaucoma. Int J Ophthalmo. 2006; 6(4): 840- 843.
3. Hiscott J, Kwon H, Genin P. Hostile takeovers: viral appropriation of the NF-κB pathway. J Clin Invest. 2001; 107(2): 143-151.
4. Danning CL, Illei GG, Hitchon C, et al. Macrophage-derived cytokine and nuclear factor kappaB p65 expression in synovial membrane and skin of patients with psoriatic arthritis. Arthritis Rheum. 2000; 43(6): 1244-1256.
5.杨政,文海泉.寻常型银屑病患者皮肤中诱生型一氧化氮合酶、核因子-κBp65表达及其临床意义.中华皮肤科杂志. 2001; 34(2): 103-104.
6. Burgos P, Metz C, Bull P, et al. Increased expression of c-re1. From the NF-kappaB/Rel family, in T cells from patients with systemic lupus erythematosus. J Rheumatol. 2000; 27 (1): 116-127.
7. Wong HK, Kammer GM, Dennis G, et al. Abnormal NF-kappa B activity in T lymphocytes from patients with systemic lupus erythematosus is associated with decreased p65-RelA protein expression. J Immunol. 1999; 163(3): 1682-1689.
8.许韩师,叶任高,孙林.系统性红斑狼疮患者外周血单一核细胞NF-κB信号通路活化检测.中华皮肤科杂志. 2001; 34(1): 18-21.
9. Li Q, Verma IM. NF-κB regulation in the immune system. Nat Rev Immunol. 2002; 2 (10): 725-734.
10. Qin JZ, Chaturvedi V, Denning MF, et al. Role of NF-κB in the apoptotic-resistant phenotype of keratinocyte. J Biol Chem. 1999; 274(53): 37957-37964.
11. Seitz CS, Freiberg RA, Hinata K, et al. NF-κB determines localization and features of cell death in epidermis. J Clin Invest. 2000; 105(3): 253-260.
12. Auphan N, DiDonato JA, Rosette C, et al. Immunosuppression by glucocorticoids: inhibition of NF-κB activity through induction of IκB synthesis. Science. 1995; 270 (5234): 286-290.
1. Krunkosky TM, Fischer BM, Martin LD, et al. Effects of TNF-alpha on expression of ICAM-1 in human airway epithelial cells in vitro. Signaling pathways controlling surface and gene expression. Am J Respir Cell Mol Biol. 2000; 22 (6): 685-692.
2.冯信忠,陆毅, Corrine L, et al.细胞因子在银屑病非皮损成纤维细胞中的表达.中华皮肤科杂志. 2003; 36 (3): 133-135.
3.王万卷,陈丽,王晓鹏.寻常型银屑病皮损中肿瘤坏死因子-α、基质金属蛋白酶9及其抑制剂-1的表达.西安交通大学学报(医学版). 2007; 28(3): 322-324.
4. Groves RW, Allen MH, Ross EL, et al. Tumor necrosis factor alpha is pro-inflammtary in normal human skin and modulates cutaneous adhesion molecule expression. Br J Dermatol. 1995; 132(3): 345-352.
5. Sheu MY, Fowler AJ, Kao J, et al. Topical peroxisome proliferators activated receptor-alpha activators reduce inflammation in irritant and allergic contant dermatitis models. J Invest Dermatol. 2002; 118(1): 94-101.
6.周伟,张建国,栗超跃. TNF-α诱导脑胶质瘤细胞凋亡过程中NF-κB、IκBα活性的研究.山东医药. 2006, 46(15): 3-4.
7. Yudt MR, Jewell CM, Bienstock RJ, et al. Molecular origins for the dominant negative function of human glucocorticoid receptor beta. Mol Cell Biol. 2003; 23(12): 4319-4330.
8. Kino T, Chrousos GP. Tumor necrosis factor alpha receptor- and Fas-associated FLASH inhibit transcriptional activity of the glucocorticoid receptor by binding to and interfering with its interaction with p160 type nuclear receptor coactivators. J Biol Chem. 2003; 278(5): 3023-3029.
9. Schaaf MJ, Cidlowski JA. AUUUA motifs in the 3, UTA of human glucocorticoid receptor alpha and beta mRNA destabilize mRNA and decrease receptor protein expression. Steroids. 2002; 67(6): 627-636.
10. Leung DY, de Castro M, Szefler SJ, et al. Mechanisms of glucocorticoid resistant asthma. Ann N Y Acad Sci. 1998; 840(6): 735-746.
11. Yudt MR, Jewell CM, Bienstock RJ, et al. Molecular origins for the dominant negative function of human glucocorticoid receptor beta. Mol Cell Biol. 2003; 23 (12): 4319-4330.
12. Pujols L, Mullol J, Picado C. Alpha and beta glucocorticoid receptors: relevance in airway diseases. Curr Allergy Asthma Rep. 2007; 7(2): 93-99.
13. Lewis-Tuffin LJ, Cidlowski JA. The physiology of human glucocorticoid receptor beta (hGRbeta) and glucocorticoid resistance. Ann N Y Acad Sci. 2006; 1069(6): 1-9.
14. Schaaf MJ, Cidlowski JA. Molecular mechanisms of glucocorticoid action and resistance. J Steroid BiochemMol Biol. 2003; 83(1): 37-48.
1.冯信忠,陆毅, Corrine L, et al.细胞因子在银屑病非皮损成纤维细胞中的表达.中华皮肤科杂志. 2003; 36 (3): 133-135.
2.王万卷,陈丽,王晓鹏.寻常型银屑病皮损中肿瘤坏死因子-α、基质金属蛋白酶9及其抑制剂-1的表达.西安交通大学学报(医学版). 2007; 28(3): 322-324.
3. Groves RW, Allen MH, Ross EL, et al. Tumor necrosis factor alpha is pro-inflammtary in normal human skin and modulates cutaneous adhesion molecule expression. Br J Dermatol. 1995; 132(3): 345-352.
4. Sheu MY, Fowler AJ, Kao J, et al. Topical peroxisome proliferators activated receptor-alpha activators reduce inflammation in irritant and allergic contant dermatitis models. J Invest Dermatol. 2002; 118(1): 94-101.
5. Ghosh S, Karin M. Missing pieces in the NF-κB puzzle. Cell. 2002; 109(Suppl): s81- s96.
6. Westergaard M, Henningsen J, Johansen C, et al. Expression and localization of peroxisome proliferators-activated receptors and nuclear factor-kappaB in BoFmal and lesional psoriatic skin. J Invest Dermatol. 2003; 121(5): 1104-1117.
7. Monici MC, Agu ennouz M, Mazzeo A, et al. Activation of nuclear factor-kappaB in inflammatory,myopathies and Duchenne muscular dystrophy. Neurology. 2003; 60(6): 993-997.
8.宋艳丽,文海泉,肖嵘,等.卡介苗多糖核酸调节特应性皮炎患者PBMC中NF-kB和Th1/Th2细胞因子的表达.中华皮肤科杂志. 2007; 40(1): 42-44.
9. Rhodus NL, Cheng B, Myers S, et al. The feasibility of monitoring NF-kappaB associated cytokines: TNF-alpha, IL-1alpha, IL-6, and IL-8 in whole saliva for the malignant transformation of oral lichen planus. Mol Carcinog. 2005; 44(2): 77-82.
10. Rhodus NL, Cheng B, Bowles W, et al. Proinflammatory cytokine levels in saliva before and after treatment of (erosive) oral lichen planus with dexamethasone. Oral Dis. 2006; 12(2): 112-116.
11. Murphy JE, Rebort C, Kupper TS. Interleukin-1 and cutaneous inflammation: a crucial ling between innate and acquired immunity. J Invest Dermatol. 2000; 114(3): 602-608.
12. Robort C, Kupper TS. Inflammatory skin diseases, T cell, and immunsurveillance. NEngl J Med. 1999; 341(24): 1817-1828.
13. Li Q, Verma IM. NF–κB regulation in the immune system. Nat Rve Immunol. 2002; 2(10): 725-734.
1. Irusen E, Matthews JG, Takahashi A, et al. p38 Mitogen-activated protein kinase-induced glucocorticoid receptor phosphorylation reduces its activity: role in steroid-insensitive asthma. J Allergy Clin Immunol. 2002, 109(4): 649-657.
2. Adcock IM, Caramori G. Cross-talk between pro-inflammatory transcription factors and glucocorticoids. Immunol Cell Biol. 2001, 79(4): 376-384.
3. Mathieu M, Gougat C, Jaffuel D, et al. The glucocorticoid receptor gene as a candidate for gene therapy in asthma. Gene Ther. 1999, 6(2): 245-252.
4. Xu Q, Leung DY, Kisich KO. Serine-arginine-rich protein p30 directs alternative splicing of glucocorticoid receptor pre-mRNA to glucocorticoid receptor beta in neutrophils. J Biol Chem. 2003, 278(29): 27112-27118.
5. Savory JG, Préfontaine GG, Lamprechtetal C, et al. Glucocorticoid Receptor Homodimers and Glucocorticoid-Mineralocorticoid Receptor Heterodimers Form in the Cytoplasm through Alternative Dimerization Interfaces. Mol Cell Biol. 2001, 21(3): 781-793.
6. Schaaf MJ, Cidlowski JA. AUUUA motifs in the 3′UTR of human glucocorticoid receptor alpha and beta mRNA destabilize mRNA and decrease receptor protein expression. Steroids. 2002, 67(7): 627-636.
7. Pujols L, Mullol J, Roca Ferrer J, et al. Expressi on of glucocorticoid receptor alpha and beta isoforms in human cells and tissues. Am J Physiol Cell Physiol. 2002, 283(4): C1324-1331.
8. Gougat C, Jaffuel D, Gagliardo R, et al. Overexpression of the human glucocorticoid receptor alpha and beta isoforms inhibits AP-1 and NF-kappaB activities hormone independently. J Mol Med. 2002, 80(5): 309-318.
9. Breslin MB, Geng CD, Vedeckis WV. Multiple promoters exist in the human GR gene, one of which is activated by glucocorticoids. Mol Endocrinol. 2001, 15 (8): 1381-1395.
10. Schottelius A, Wedel S, Weltrich R, et al. Higher expression of glucocorticoid receptor in peripheral mononuclear cells in inflammatory bowel disease. Am J Gast roenterol. 2000, 95(8): 1994-1999.
11. Webster JC, Oakley RH, Jewell CM, et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance. Proc Natl Acad Sci USA. 2001, 98(12): 6865-6870.
12. Cho YJ, Lee KE. Decreased glucocorticoid binding affinity to glucocorticoid receptor is important in the poor response to steroid therapy of older-aged patients with severe bronchial asthma. Allergy Asthma Proc. 2003, 24(5): 353-358.
13. Pujols L, Xaubet A, Ramirez J, et al. Expression of glucocorticoid receptors alpha and beta in steroid sensitive and steroid insensitive interstitial lung diseases. Thorax. 2004, 59(8): 687-693.
14. Oakley RH, Jewell CM, Yudt MR, et al. The dominant negative activity of the human glucocorticoid receptor beta isoform. Specificity and mechanisms of action. J Biol Chem. 1999, 274(39): 27857-27866.
15. Sousa AR, Lane SJ, Cidlowski JA, et al. Glucocorticoid resistance in asthma is associated with elevated in vivo expression of the glucocorticoid receptor beta-isoform. J Allergy Clin Immunol. 2000, 105(5): 943-950.
16. Honda M, Orii F, Ayabe T, et al. Expression of glucocorticoid receptor beta in lymphocytes of patients with glucocorticoid-resistant ulcerative colitis. Gastroenterology. 2000, 118(5): 859-866.
17. Chikanza IC. Mechanisms of corticosteroid resistance in rheumatoid arthritis: a putative role for the corticosteroid receptor beta isoform. Ann N Y Acad Sci. 2002, 966(7): 39-48.
18. Gagliardo R, Chanez P, Vignola AM, et al. Glucocorticoid receptor alpha and beta in glucocorticoid dependent asthma. Am J Respir Crit Care Med. 2000, 162(1): 7-13.
19. Goebels N, Michaelis D, Engelhardt M, et al. Diferential expression of perform in muscle infiltrating T cells in polymyositis and dermatomyositis. J Clin Invest. 1996, 97(12): 2905-2910.
20. El-Naghy M, Johnson BH, Chen H, et al. The pathway of leukemic cell death caused by glucocorticoid receptor fragment 465*. Exp Cell Res. 2001, 270(2): 165-175.
21. Chikanza IC. Mechanisms of corticosteroid resistance in rheumtoid arthritis: a putative role for the corticosteroid receptor beta isoform. Ann NY Acad Sci. 2002, 966(7): 39-48.
22.赵玉华,刘秉文.核因子-κB糖皮质激素受体途径的拮抗作用.生理科学进展. 2003,33(3): 261-264.
23. Efthimiou P, Schwartzman S, Kagen LJ. Possible role for tumour necrosis factor inhibitors in the treatment of resistant dermatomyositis and polymyositis: a retrospective study of eight patients. Ann Rheum Dis. 2006, 65(9): 1233-1236.
24. Ramanan AV, Campbell-Webster N, Ota S, et al. The effectiveness of treating juvenile dermatomyositis with methotrexate and aggressively tapered corticosteroids. Arthritis Rheum. 2005, 52(11): 3570-3578.
25. Edge JC, Outland JD, Dempsey JR, et al. Mycopheno1ate mofetil as an effective corticosteroid-sparing therapy for recalcitrant dermatomyositis. Arch Dermatol. 2006, 142(1): 65-69.
26.陈向芳,林炜栋,张汝芝,等.多发性肌炎/皮肌炎患者糖皮质激素受体与微量元素的改变及意义.第二军医大学学报. 2007, 28(7): 793-795.
27. De Bleecker JL, De Paepe B, Vervaet VL, et al. Distribution of glucocorticoid receptor alpha and beta subtypes in the idiopathic inflammatory myopathies. Neuromuscul Disord. 2007, 17(2): 186-193.
28. Stuerenburg HJ, Kunze K. Glucocorticoid receptor concentrations in muscle biopsies from patients with neuromuscular diseases. Eur J Neurol. 1999, 6(4): 469-472.
29. Bamberger CM, Bamberger AM, De Castro M, et al. Glucocorticoid receptorβ, a potential endogenous inhibitor of glucocorticoid action in humans. J Clin Invest. 1995, 95(6): 2435-2441.
30. Goebels N, Michaelis D, Engelhardt M, et al. Differential expression of perforin in muscle-infiltrating T cells in polymyositis and dermatomyositis. J Clin Invest. 1996, 97(12): 2905-2910.
31.刘继峰,李久宏,翟宁,等.多发性肌炎/皮肌炎患者外周血单一核细胞中糖皮质激素受体及热休克蛋白90 mRNA的表达.中华皮肤科杂志. 2004, 37(1): 52.
32.刘继峰,许爱娥,宋芳吉,等.多发性肌炎/皮肌炎患者外周血单个核细胞中糖皮质激素受体α、βmRNA表达与糖皮质激素疗效相关性的研究.中国免疫学杂志. 2007, 23(4): 364-367.
33.宋亮年.甾体激素受体家族.见:卢建,余应年,徐仁宝,主编.受体信号转导系统与疾病.济南:山东科学技术出版社, 1999, 370-381.
34. Wilkens T, De Rijk R. Glucocorticoids and immune function: unknown dimensions andnew frontiers. Immunology Today. 1997, 18(9): 418-412.
35. Miller AH, Spencer RL, Pearce BD, et al. Glucocorticoid receptors are differentially expressed in the cells and tissues of the immune system. Cell Immuno. 1998, 186(1): 45-54.
36.梅冰,康舟军,杨瑞和,等.创伤性休克大鼠中性粒细胞CD18和糖皮质激素受体的变化及纳络酮的治疗作用.中国危重病急救医学. 1999, 11(6): 364-367.
37.林海,肖素芳,林忠清,等.糖皮质激素受体减少对严重烫伤大鼠体内炎症介质水平的影响.中国病理生理杂志. 2000, 16(1): 60-62.
38.李志军,余裕民,李兴福,等.系统性红斑狼疮患者外周血白细胞糖皮质激素受体结合量测定的临床意义.中华风湿病学杂志. 2005, 9(10): 597-600.
39.李久宏,高奎斌,韩秀萍,等.狼疮性肾炎患者外周血单个核细胞中糖皮质激素受体和热休克蛋白90 mRNA表达的研究.中华微生物学和免疫学杂志. 2003, 23(9): 727.
40.李秀,张凤山,李英楠.糖皮质激素受体α在系统性红斑狼疮发病机制中的作用研究.中华风湿病学杂志. 2006, 10(5): 290-293.
41.李久宏,李波,毕桂姣.系统性红斑狼疮患者糖皮质激素及受体mRNA相关性研究.中华皮肤科杂志. 2004, 37(1): 48-49.
42. Jiang T, Liu S, Tan M, et al. The phase-shift mutation in the glucocorticoid receptor gene: potential etiologic significance of neuroendocrine mechanisms in lupus nephritis. Clin Chim Acta. 2001, 313(1-2): 113-117.
43. Ginsberg ZH. Psychophysiological aspects of psoriasis. Dermatol Clin. 1995, 13 (5): 793-803.
44.杨雪琴,彭德河,许传珊,等.银屑病患者的性格及情感分析.中华皮肤科杂志. 1991, 24 (1): 33-34.
45.徐仁宝.休克时糖皮质激素受体的变化及大剂量糖皮质激素抗休克治疗的受体机制.基础医学与临床. 1998, 18(1): 5-10.
46. Weigl BA. Immuno regulatory mechanism and stress hormones in psoriasis. Int J Dermatol. 1998, 37(3): 350-357.
47.樊建勇,杨雪琴,张力军,等.银屑病患者血中糖皮质激素及其受体mRNA的测定及其意义.第四军医大学学报. 2001, 22 (22): 2091-2093.
48.韩良辅,肖华胜,陈景藻.次声作用引起大鼠下丘脑c-fos mRNA与CRF mRNA的表达.第四军医大学学报. 1999, 20(1): 1-3.
49. Karalis K, Sano H, Redwine J, et al. Autocrine or paracrine inflammatory actions of CRH in vivo. Science. 1991, 254 (5): 421-423.
50. Gunduz K, Ozturk G, Terzioglu E, et al. T cell subpopulations and IL-2R in vitiligo. J Dermato1. 2004, 31(2): 94-97.
51. Steitz J, Bruck J, Lenz J, et al. Peripheral CD8+ T cell tolerance against melanocytic self-antigens in the skin is regulated in two steps by CD4+ T cells and local inflammation: mplications for the pathophysiology of vitiligo. J Invest Dermatol. 2005, 124 (1): 144-150.
52. Mandelcom-Monson RL, Shear NH, Yau E, et al. Cytotoxic T lymphocyte reactivity to gpl00, MelanA/MART-1, and tyrosinase, in HLA-A2-positive vitiligo patients. J Invest Dermatol. 2003, 121(3): 550-556.
53. Kroll TM, Bommiasamy H, Boissy RE, et al. 4-Tertiary butyl phenol exposure sensitizes human melanocytes to dendritic cell-mediated killing: relevance to vitiligo. J Invest Dermatol. 2005, 124(4): 798-806.
54. Daneshpazhooh M, Mostofizadeh GM, Behjati J, et al. Anti-thyroid peroxidase antibody and vitiligo: a controlled study. BMC Dermatol. 2006, 6:3.
55. Blomhof A, Kemp EH, Gawkrodger DJ, et al. CTLA4 polymorphisms are associated with vitiligo, in patients with concomitant autoimmune diseases. Pigment Cell Res. 2005, 18(1): 55-58.
56.许清玉,卢念祖,韩建德.糖皮质激素受体在白癜风患者外周血单核细胞中的表达.临床皮肤科杂志. 2007, 36(8): 491-492.
1. Hiscott J, Kwon H, Genin P. Hostile takeovers: viral appropriation of the NF-κB pathway. J Clin Invest. 2001, 107(2): 143-151.
2. Viatour P, Merville MP, Bours V, et al. Phosphorylation of NF-kappa B and I kappa B protein: implications in cancer and inflammation. Trends Biochem Sci. 2005, 30(1): 43-52.
3. Huguet C, Crepieux P, Laudet V. Rel/NF-κB transcription factors and IκB inhibtors: evolution from a unique common ancestor. Oncogene. 1997, 15(24): 2965-2974.
4. Simeonidis S, Stauber D, Chen GY, et al. Mechanisms by which IκB proteins control NF-κB activity. Biochemistry. 1999, 96(1): 49-54.
5. Whiteside ST, Israel A. IκB proteins: structure, function and regulation. Cancer Biol. 1997, 8(2): 75-82.
6. May MJ, Ghosh S. Rel/NF-κB and IκB proteins: an overview. Cancer Biol. 1997, 8(2): 63-73.
7. Chang NS. The non-ankyrin C terminus of IκBαphysically interacts with p53 in vivo and dissociates in response to apoptotic stress, hypoxia, DNA damage, and transforming growth factor-β1-mediated growth suppression. J Biol Chem. 2002, 277(12): 10323-10331.
8. Takaesu G, Surabhi RM, Park KJ, et al. TAK1 is critical for I kappa B kinase-mediated activation of the NF-kappa B pathway. J Mol Biol. 2003, 326 (1): 105-115.
9. Yamazaki S, Muta T, Takeshige K. A novel IκB protein, IκB-zeta, induced by proinflammatory stimuli, negatively regulates nuclear factor-κB in the nuclei. J Biol Chem. 2001, 276(29): 27657-27662.
10. Karin M, Delhase M. The I kappa B kinase (IκK) and NF-kappa B: key elements of proinflammatory signalling. Semin Immunol. 2000, 12(1): 85-98.
11. Yang F, Tang E, Guan K, et al. Iκk beta plays an essential role in the phosphorylation of ReLA/p65 on serine 536 induced by lipopolysaccharide. Immunol. 2003, 170(11): 5630-5635.
12. Li Q, Verma IM. NF–κB regulation in the immune system. Nat Rve Immunol. 2002,2(10): 725-734.
13. Bell S, Degitz K, QuirlingM, et al. Involvement of NF-kappacB signalling in skin physiology and disease. Cell Signal. 2003, 15(1):1-7.
14. Robert C, Kupper TS. Inflammatory skin diseases, T cells, and immune surveillance. N Engl J Med. 1999, 341(24): 1817-1828.
15.郁博,陈德宇,何威.与银屑病发病相关的某些细胞因子.中国麻风皮肤病杂志. 2007, 23(8): 696-698.
16. Danning CL, Illei GG, Hitchon C, et al. Macrophage-derived cytokine and nuclear factor kappaB p65 expression in synovial membrane and skin of patients with psoriatic arthritis. Arthritis Rheum. 2000, 43(6): 1244-1256.
17.杨政,文海泉.寻常型银屑病患者皮肤中诱生型一氧化氮合酶、核因子-κBp65表达及其临床意义.中华皮肤科杂志. 2001, 34(2): 103-104.
18. Bos JD, De Rie MA. The pathogenesis of psoriasis: immunological facts and speculations. Immunol Today. 1999, 20(1): 40-46.
19. Baldwin AS. Control of oncogenesis and cancer therapy resistance by the transcription factor NF-kappaB. J Clin Invest. 2001, 107(1): 241-246.
20. Westergaard M, Henningsen J, Johansen C, et al. Expression and localization of peroxisome proliferators-activated receptors and nuclear factor-kappaB in normal and lesional psoriatic skin. J Invest Dermatol. 2003, 121(5): 1104-1117.
21 Zollner TM, Podda M, Picn C. Proteasome inhibition reduces superantigen-mediaed T cell activation and the severity of psoriasis in a SCID-hu model. J Clin Invest. 2002, 109 (5): 671-679.
22 Tak PP, Firestein GS. NF-kappa B: a key role in inflammatory disease. J Clin Invest. 2001, 107(1): 7-11.
23 Kovacich JC, Boyle EM, Morgan EN, et al. Inhibition of the transcriptional activator protein nuclear factor kappa B prevents hemodynamic instability associated with the whole-body inflammatory response syndrome. J Thorac Cardiovasc Surg. 1999, 118(1): 154-162.
24 Becker H, Stengl G, Stein M, et al. Analysis of proteins that interact with the IL-2 regulatory region in patients with rheumatic diseases. Clin Exp Immunol. 1995, 99(3): 325-330.
25 Monici MC, Aguennouz M, Mazzeo A, et al. Activation of nuclear factor-kappa B in inflammatory, myopathies and Duchenne muscular dystrophy. Neurology. 2003, 60(6): 993-997.
26 Burgos P, Metz C, Bull P, et al. Increased expression of c-re1 From the NF-kappaB/Rel family, in T cells from patients with systemic lupus erythematosus. J Rheumatol. 2000, 27(1): 116-127.
27 Wong HK, Kammer GM, Dennis G, et al. Abnormal NF-kappa B activity in T lymphocytes from patients with systemic lupus erythematosus is associated with decreased p65-RelA protein expression. J Immunol. 1999, 163(3): 1682-1689.
28许韩师,叶任高,孙林.系统性红斑狼疮患者外周血单一核细胞NF-κB信号通路活化检测.中华皮肤科杂志. 2001, 34(1): 18-21.
29 Novak N, Valenta R, Bohle B, et al. Fc(epsilon)RI engagement of Langerhans cell-like dendritic cells and inflammatory dendritic epidermal cell-like dendritic cells induces chemotactic signals and different T-cell phenotypes in vitro. J Allergy Clin Immunol. 2004, 113(5): 949-957.
30宋艳丽,文海泉,肖嵘,等.卡介苗多糖核酸调节特应性皮炎患者PBMC中NF-kB和Th1/Th2细胞因子的表达.中华皮肤科杂志. 2007, 40(1): 42-44.
31谢志强,刘玲玲,窦侠,等.特应性皮炎皮损角质形成细胞NF-κB表达及外用他克莫司对其的影响.北京大学学报(医学版). 2004, 36(5): 487-490.
32 Kaburagi Y, Shimada Y, Nagaoka T, et al. Enhanced production of CC-chemokines (RANTES, MCP-1. MIP-l alpha, MIP-l beta, and eotaxin) in patients with atopic dermatitis. Arch Dermatol Res. 2001, 293(7): 350-355.
33 Huber MA, Denk A, Peter RU, et al. The IKK-2/I kappa B alpha/NF-kappa B pathway plays a key role in the regulation of CCR3 and Eotaxin-l in fibroblasts. A critical link to dermatitis in I kappa Bat-Pha-deficient mice. J Biol Chem. 2002, 277(2): 1268-1275
34 Kim JH, Ha IS, Hwang CI, et al. Gene expression profiling of anti-GBM glomerulonephritis model: the role of NF-kappa B in immune complex kidney disease. Kidney Int. 2004, 66(5): 1826-1837.
35 Baouz S, Giron-Michel J, Azzarone B, et al. Lung myofibroblasts as targets of salmeterol and fluticasone propionate: inhibition of alpha-SMA and NF-kappa B. Int Immunol. 2005, 17(11): 473-1481.
36 Yousaf N, Gould DJ, Aganna E, et al. Tumor necrosis factor receptor I from patients with tumor necrosis factor receptor-associated periodic syndrome interacts with wild-type tumor necrosis factor receptor I and induces ligand-independent NF-kappa B activation. Arthritis Rheum. 2005, 52(9): 2906-2916.
37 Kraft S, Novak N, Katoh N, et al. Aggregation of the high-affinity IgE receptor Fc (epsilon) RI on human monocytes and dendritic cells induces NF-kappa B activation. J Invest Dermatol. 2002, 118(5): 830-837.
38 Nakamura H, Aoki M, Tamai K, et al. Prevention and regression of atopic dermatitis by ointment containing NF-kB decoy oligodeoxynucleotides in NC/Nga atopic mouse model. Gene Ther. 2002, 9(18): 1222-1229.
39 Abeyama K, Eng W, Jester JV, et al. A role for NF-kappa B-dependent gene transactivation in sunburn. J Clin Invest. 2000, 105(12): 1751-1759.
40 Djavaheri Mergny M, Gras MP, Mergny JL, et al. UVA-induced decrease ill nuclear factor-kappaB activity in human keratinocytes. Biochem J. 1999, 338(3): 607-613.
41 Gilmore TD. NF-kappa B is required for H-ras oncogene induced abnormal cell proliferation and tumorigenesis. Oncogene, 2000, 19(7): 841-849.
42 Hinz M, Krappmann D, Eichten A, et al. Nuclear factor-kappa B, cancer, and apoptosis. Mol Cell Biol. 2004, 64(4): 2690-2698.
43 Kaltschmidt B, Kaltschmidt C, Hehner SP, et al. An approach to proteomic analysis of human tumors. Oncogene. 2003, 22(49): 3213-3215.
44 Kiernan R, Bres V, Ng RW, et al. Post-activation turn-off of NF-kappa B-dependent transcription is regulated by acetylation of p65. J Biol Chem. 2003, 278(4): 2758–2766.
45 Digicaylioglu M. Erythropoietin-mediated neuroprotection involves cross-talk between Jak-and NF-κB signaling cascades. Nature. 2001, 412(6847): 641–647.
46 Tamatani M, Mitsuda N, Matsuzaki H, et al. A pathway of neuronal apoptosis induced by hypoxia Preoxygenation: roles of nuclear factor-kappa B and Bcl-2. J Neurochem. 2000, 75(2): 683-693.
47 Foo SY, Nolan GP. Genetic approachs in mice to understand NF-kappa B function. Trends Genet. 2003, 18(6): 229-235.
48 Ciana P, Neri A, Cappellini C, et al. Constitutive expression of lymphoma-associated NFKB-2/Ly1-10 proteins is tumorigenic in murine fibroblasts. Oncogene. 1997, 14(15):1805-1810.
49 Dejardin E, Deregowski V, Chepelier M, et al. The nuclear factor-kappa B: a protential therapeutic target for cancers. Oncogene. 2003, 22(49): 2567-2577.
50 Nakayama H, Ikebe T, Beppu M, et al. High expression levels of nuclear factor kappa B, I kappa B kinase alpha and Akt kinase in squamous cell carcinoma of the oral cavity. Cancer. 2001, 92(12): 3037-3044.
51 Budunova IV, Perez P, Vaden VR, et al. Increased expression of p50 NF-kappa B and constitutive activation of NF-kappa B transcription factors during mouse skin carcinogenesis. Oncogene. 1999, 18(52): 7423-7431.
52 Hodgson L, Henderson AJ, Dong C. Melanoma cell migration to type IV collagen requires activation of NF-kappa B. Oncogene. 2003, 22(1): 98-108.
53 Kashani Sabet M, Liu Y, Fong S, et al. Identification of gene function and functional pathways by systetmic plasmid-based ribozyme targeting in adult mice. Proc Natl Acad Sci USA. 2002, 99(6): 3878-3883.
54 Izaban KF, Ergin M, Qin JZ, et al. Constitutive expression of NF-κB is a characteristic feature of mycosis fungoides: implications for apoptosis resistance and pathogenesis. Hum Pathol. 2000, 31(12): 1482-1490.
55王海林,侯建新,周桂芝,等.皮肤淋巴瘤中c-myb和NF-κB的表达及意义.中国麻风皮肤病杂志. 2007, 23(5): 384-387.
56 Aradhya S, Wofiendin H, Jakins T, et al. A recurrent deletion in the ubiquitously expressed NEMO(IKK-gamma) gene accounts for the vast majority of incontinentia pigmenti mutations. Hum Mol Genet. 2001, 10(19): 2171-2179.
57 Smahi A, Courtois G, Rabia SH, et al. The NF-kappa B signaling pathway in human diseases: from incontinentia pigmenti to ectodermal dysplasias and immune-deficiency syndromes. Hum Mol Genet. 2002, 11(20): 2371-2375.
58 Santoro A, Majorana A, Bardellini E, et al. NF-kappa B expression in oral and cutaneous lichen planus. Pathol. 2003, 201(3): 466-472.
59 Rhodus NL, Cheng B, Myers S, et al. The feasibility of monitoring NF-kappa B associated cytokines: TNF-alpha, IL-1alpha, IL-6, and IL-8 in whole saliva for the malignant transformation of oral lichen planus. Mol Carcinog. 2005, 44(2): 77-82.
60 Rhodus NL, Cheng B, Bowles W, et al. Proinflammatory cytokine levels in saliva before and after treatment of (erosive) oral lichen planus with dexamethasone. Oral Dis. 2006, 12(2): 112-116.
61任晓丽,白莉.核因子κB、细胞间黏附分子1在扁平苔藓中的表达和意义.中国麻风皮肤病杂志. 2007, 23(7): 596-598.
2. Duma D, Jewell CM, Cidlowski JA. Multiple glucocorticoid receptor isoforms and mechanisms of post-translational modification. J Steroid BiochemMol Biol. 2006; 102(1-5): 11-21.
3. Schaaf MJ, Cidlowski A. Molecular mechanisms of glucocorticoid action and resistance. J Steroid BiochemMol Biol. 2003; 83(1): 37-48.
4. Cho YJ, Lee KE. Decreased glucocorticoid binding affinity to glucocorticoid receptor is important in the poor response to steroid therapy of older-aged patients with severe bronchial asthma. Allergy Asthma Proc. 2003, 24(5): 353-358.
5. Pujols L, Xaubet A, Ramirez J, et al. Expression of glucocorticoid receptors alpha and beta in steroid sensitive and steroid insensitive interstitial lung diseases. Thorax. 2004; 59(8): 687-693.
6. Raddatz D, Middel P, Bockemuhl M. Glucocorticoid receptor expression in inflammatory bowel disease: evidence for a mucosal down-regulation in steroid-unresponsive ulcerative colitis. Aliment Pharmacol Ther. 2004; 19(1): 47-61.
7. Yudt MR, Jewell CM, Bienstock RJ, et al. Molecular origins for the dominant negative function of human glucocorticoid receptor beta. Mol Cell Biol. 2003; 23(12): 4319-4330.
8. Pujols L, Mullol J, Picado C. Alpha and beta glucocorticoid receptors: relevance in airway diseases. Curr Allergy Asthma Rep. 2007; 7(2): 93-99.
9. Lewis-Tuffin LJ, Cidlowski JA. The physiology of human glucocorticoid receptor beta (hGRbeta) and glucocorticoid resistance. Ann N Y Acad Sci. 2006; 1069(6): 1-9.
10. Lu N, Cidlowski J. The origin and functions of multiple human glucocorticoid receptor isoforms. Ann N Y Acad Sci. 2004; 1024 (6): 102-123.
11.杨玲,何威,黎智,等。糖皮质激素受体α、核因子-κB、肿瘤坏死因子-α和白介素-1β在慢性皮炎中的表达.临床皮肤科杂志, 2006, 35(5): 291-293.
12. Ghosh S, Karin M. Missing pieces in the NF-κB puzzle. Cell. 2002; 109(Suppl): s81-s96.
13. Li Q, Verma IM. NF-κB regulation in the immune system. Nat Rev Immunol. 2002; 2 (10): 725-734.
14. Qin JZ, Chaturvedi V, Denning MF, et al. Role of NF-κB in the apoptotic-resistant phenotype of keratinocyte. J Biol Chem. 1999; 274(53): 37957-37964.
15. Seitz CS, Freiberg RA, Hinata K, et al. NF-κB determines localization and features of cell death in epidermis. J Clin Invest. 2000; 105(3): 253-260.
16. Auphan N, DiDonato JA, Rosette C, et al. Immunosuppression by glucocorticoids: inhibition of NF-κB activity through induction of IκB synthesis. Science. 1995; 270 (5234): 286-290.
17. Westergaard M, Henningsen J, Johansen C, et al. Expression and localization of peroxisome proliferators-activated receptors and nuclear factor-kappaB in BoFmal and lesional psoriatic skin. J Invest Dermatol. 2003; 121(5): 1104-1117.
18. Monici MC, Agu ennouz M, Mazzeo A, et al. Activation of nuclear factor-kappaB in inflammatory,myopathies and Duchenne muscular dystrophy. Neurology. 2003; 60(6): 993-997.
19.宋艳丽,文海泉,肖嵘,等.卡介苗多糖核酸调节特应性皮炎患者PBMC中NF-kB和Th1/Th2细胞因子的表达.中华皮肤科杂志. 2007; 40(1): 42-44.
20. Rhodus NL, Cheng B, Myers S, et al. The feasibility of monitoring NF-kappaB associated cytokines: TNF-alpha, IL-1alpha, IL-6, and IL-8 in whole saliva for the malignant transformation of oral lichen planus. Mol Carcinog. 2005; 44(2): 77-82.
21. Rhodus NL, Cheng B, Bowles W, et al. Proinflammatory cytokine levels in saliva before and after treatment of (erosive) oral lichen planus with dexamethasone. Oral Dis. 2006; 12(2): 112-116.
22. Murphy JE, Rebort C, Kupper TS. Interleukin-1 and cutaneous inflammation: a crucial ling between innate and acquired immunity. J Invest Dermatol. 2000; 114(3): 602-608.
23. Robort C, Kupper TS. Inflammatory skin diseases, T cell, and immunsurveillance. N Engl J Med. 1999; 341(24): 1817-1828.
24.冯信忠,陆毅, Corrine L, et al.细胞因子在银屑病非皮损成纤维细胞中的表达.中华皮肤科杂志. 2003; 36 (3): 133-135.
25.王万卷,陈丽,王晓鹏.寻常型银屑病皮损中肿瘤坏死因子-α、基质金属蛋白酶9及其抑制剂-1的表达.西安交通大学学报(医学版). 2007; 28(3): 322-324.
26. Groves RW, Allen MH, Ross EL, et al. Tumor necrosis factor alpha is pro-inflammtary in normal human skin and modulates cutaneous adhesion molecule expression. Br J Dermatol. 1995; 132(3): 345-352.
27. Sheu MY, Fowler AJ, Kao J, et al. Topical peroxisome proliferators activated receptor-alpha activators reduce inflammation in irritant and allergic contant dermatitis models. J Invest Dermatol. 2002; 118(1): 94-101.
28. Kino T, Chrousos GP. Tumor necrosis factor alpha receptor- and Fas-associated FLASH inhibit transcriptional activity of the glucocorticoid receptor by binding to and interfering with its interaction with p160 type nuclear receptor coactivators. J Biol Chem. 2003; 278(5): 3023-3029.
29. Webster JC, Oakley RH, Jewell CM, et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance. Proc Natl Acad Sci. 2001; 98(12): 6865-6870.
1.陈锡唐,等.实用皮肤组织病理学.广州:广东科技出版社. 1994: 163-168.
2.杨玲,何威,黎智,等.糖皮质激素受体α、核因子-κB、肿瘤坏死因子-α和白介素-1β在慢性皮炎中的表达.临床皮肤科杂志. 2006; 35(5): 291-293.
3.王志红,肖素芳,林海,等.烫伤大鼠糖皮质激素受体减少与全身炎症反应综合征的关系.福建医科大学学报. 2000; 34(1): 39-40.
4. Cidlowski JA, Cidlowski NB. Regulation of glucocorticoid receptors by glucocorticoids in cultured HeLa S3 cells. Endocrinology. 1981; 109(6): 1975-1982.
5. Svec F, Rudis M. Glucocorticoids regulate the glucocorticoid receptor in the AtT20 cell. J Biol Chem. 1981; 256(12): 5984-5987.
6. Danielsen M, Stallcup M. Down-regulation of the glucocorticoid receptor in mouse lymphoma cell variants. Mol Cell Biol. 1984; 4(3): 449-453.
7. Silva C, Powell-Oliver F, Cidlowski J. Regulation of the human glucocorticoid receptor by long-term and chronic treatment with glucocorticoids. Steroids. 1994; 59(7): 436-442.
8. Dong Y, Poellinger L, Gustafsson J, et al. Regulation of the glucocorticoid receptor expression: Evidence for transcriptional and posttranslational mechanisms. Mol Endocrin. 1988; 2(12): 1256-1264.
9. Burnstein K, Jewell C, Cidlowski J. Human glucocorticoid receptor cDNA contains sequences sufficient for receptor down-regulation. J Biol Chem. 1990; 265(13): 7284-7291.
10. Burnstein K, Bellingham D, Jewell C, et al. Autoregulation of glucocorticoid receptor gene expression. Steroids. 1991; 56(2): 52-58.
11. Bellingham D, Sar M, Cidlowski J. Ligand-dependent downregulation of stably transfected glucocorticoid receptors is associated with the loss of functional glucocorticoid responsiveness. Mol Endocrinol. 1992; 6(12): 2090-2102.
12. Hoeck W, Rusconi S, Groner B. Down-regulation and phosphorylation of the glucocorticoid receptors in cultured cells. Investigations with a monospecific antiserumagainst a bacterially expressed receptor fragment. J Biol Chem. 1989; 264(24): 14396-14402.
13. Vachier I, Chiappara G, Vignola AM, et al. Glucocorticoid receptors in bronchial epithelial cells in asthma. Am J Respir Crit Care Med. 1998; 158(3): 963-970.
14. Karl M, Lamberts SW, Detera-Wadleigh SD, et al. Familial glucocorticoid resistance caused by a splice site deletion in the human glucocorticoid receptor gene. J Clin Endocrinol Metab. 1993; 76(3): 683-689.
15. Adcock IM. Steroid resistance in asthma. Molecular mechanisms.Am J Respir Crit Care Med. 1996; 154(2 Pt 2): S58–61.
1.杨玲,何威,黎智,等.糖皮质激素受体α、核因子-κB、肿瘤坏死因子-α和白介素-1β在慢性皮炎中的表达.临床皮肤科杂志. 2006; 35(5): 291-293.
2. Xu M, Song L, Wang Z. Effects of Dexamethasone on glucocorticoid receptor expression in a human ovarian carcinoma cell line 3AO. Chin Med J (Engl). 2003; 116(3): 392-395.
3.李波,白祥军,王海平.地塞米松对人单核细胞糖皮质激素受体蛋白表达的影响.中华急诊医学杂志. 2006; 15(6): 525-528.
4. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and 2 (-Delta Delta C (T). Methods. Methods, 2001; 25(4): 402-408.
5. Pace TW, Hu F, Miller AH. Cytokine-effects on glucocorticoid receptor function: relevance to glucocorticoid resistance and the pathophysiology and treatment of major depression. Brain Behav Immun. 2007; 21(1): 9-19.
6. Duma D, Jewell CM, Cidlowski JA. Multiple glucocorticoid receptor isoforms and mechanisms of post-translational modification. J Steroid BiochemMol Biol. 2006; 102(1-5): 11-21.
7. Schaaf MJ, Cidlowski A. Molecular mechanisms of glucocorticoid action and resistance. J Steroid BiochemMol Biol. 2003; 83(1):37-48.
8. Albrecht M, Janssen M, Konrad L, et al. Effects of dexamethasone on proliferation of and fibronectin synthesis by human primary prostatic stromal cells in vitro. Andrologia. 2002; 34(1): 11-21.
9. Cho YJ, Lee KE. Decreased glucocorticoid binding affinity to glucocorticoid receptor is important in the poor response to steroid therapy of older-aged patients with severe bronchial asthma. Allergy Asthma Proc. 2003; 24(5): 353-358.
10. Pujols L, Xaubet A, Ramirez J, et al. Expression of glucocorticoid receptors alpha and beta in steroid sensitive and steroid insensitive interstitial lung diseases. Thorax. 2004; 59(8): 687-693.
11. Raddatz D, Middel P, Bockemuhl M. Glucocorticoid receptor expression in inflammatory bowel disease: evidence for a mucosal down-regulation in steroid-unresponsive ulcerative colitis. Aliment Pharmacol Ther. 2004; 19(1): 47-61.
12. Yudt MR, Jewell CM, Bienstock RJ, et al. Molecular origins for the dominant negative function of human glucocorticoid receptor beta. Mol Cell Biol. 2003; 23(12): 4319-4330.
13. Pujols L, Mullol J, Picado C. Alpha and beta glucocorticoid receptors: relevance in airway diseases. Curr Allergy Asthma Rep. 2007; 7(2): 93-99.
14. Lewis-Tuffin LJ, Cidlowski JA. The physiology of human glucocorticoid receptor beta ( hGRbeta ) and glucocorticoid resistance. Ann N Y Acad Sci. 2006; 1069(6): 1-9.
15. Webster JC, Oakley RH, Jewell CM, et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance. Proc Natl Acad Sci. 2001; 98(12): 6865-6870.
16. Lu N, Cidlowski J. The origin and functions of multiple human glucocorticoid receptor isoforms. Ann N Y Acad Sci. 2004; 1024 (6): 102-123.
1. Minguet S, Huber M, Rosenkranz L. Adenosine and cAMP are potent inhibitors of the NF-kappa B pathway downstream of immunoreceptors. Eur J Immunol. 2005; 35(1): 31-41.
2. Zhang Q, Li PH. Research advances on relationship between nudear factor-kB and glaucoma. Int J Ophthalmo. 2006; 6(4): 840-843.
3. Gavrilyuk V, Dello Russo C, Heneka MT, et al. Norepinephrine increases I kappa B alpha expression in astrocytes. J Biol Chem. 2002; 277(33): 29662-29668.
4. Livak KJ, Schmittgen TD. Analysis of relative gene expression data using real-time quantitative PCR and 2-Delta Delta C (T). Methods. Methods. 2001; 25(4): 402-408.
5. Mori NF, Shirakawa H, Shimizu S, et al. Transcriptional regulation of the human interleukin-6 gene promoter in human T cell leukem ia virus typeéinfected T cell lines: evidence for the involvement of NF-кB. Blood. 1994; 84(9): 2904-2914.
6. Ghosh S, Karin M. Missing pieces in the NF-κB puzzle. Cell, 2002; 109(Suppl): s81-s96.
7. Li Q, Verma IM. NF-κB regulation in the immune system. Nat Rev Immunol. 2002; 2 (10): 725-734.
8. Qin JZ, Chaturvedi V, Denning MF, et al. Role of NF-κB in the apoptotic-resistant phenotype of keratinocyte. J Biol Chem. 1999; 274(53): 37957-37964.
9. Seitz CS, Freiberg RA, Hinata K, et al. NF-κB determines localization and features of cell death in epidermis. J Clin Invest. 2000; 105(3): 253-260.
10. Auphan N, DiDonato JA, Rosette C, et al. Immunosuppression by glucocorticoids: inhibition of NF-κB activity through induction of IκB synthesis. Science. 1995; 270 (5234): 286-290.
11. Westergaard M, Henningsen J, Johansen C, et al. Expression and localization of peroxisome proliferators-activated receptors and nuclear factor-kappaB in BoFmal and lesional psoriatic skin. J Invest Dermatol. 2003; 121(5): 1104-1117.
12. Monici MC, Agu ennouz M, Mazzeo A, et al. Activation of nuclear factor-kappaB in inflammatory,myopathies and Duchenne muscular dystrophy. Neurology. 2003; 60(6): 993-997.
13.宋艳丽,文海泉,肖嵘,等.卡介苗多糖核酸调节特应性皮炎患者PBMC中NF-kB和Th1/Th2细胞因子的表达.中华皮肤科杂志. 2007; 40(1): 42-44.
14. Rhodus NL, Cheng B, Myers S, et al. The feasibility of monitoring NF-kappaB associated cytokines: TNF-alpha, IL-1alpha, IL-6, and IL-8 in whole saliva for the malignant transformation of oral lichen planus. Mol Carcinog. 2005; 44(2): 77-82.
15. Rhodus NL, Cheng B, Bowles W, et al. Proinflammatory cytokine levels in saliva before and after treatment of (erosive) oral lichen planus with dexamethasone. Oral Dis. 2006; 12(2): 112-116.
16. Tao Y, Williams-Skipp C, Scheinman RI. Mapping of glucocorticoid receptor DNA binding domain surfaces contributing to transrepression of NF-kappa B and induction of apoptosis. J Biol Chem. 2001; 276(4): 2329-2332.
17. Deroo BJ, Archer TK. Glucocorticoid receptor activation of the I kappa B alpha promoter within chromatin. Mol Biol Cell. 2001; 12(11): 3365-3374.
18. Brostjan C, Anrather J, Csizmadia V, et al. Glucocorticoid–mediated repression of NF-kappaB activity in endothelial cells does not involve induction of I-kappaB alpha synthesis. J Biol Chem. 1996; 271(32): 19612-19616.
1. Bray PJ, Cotton RG. Variations of the human glucocorticoid receptor gene (NR3C1): pathological and in vitro mutations and polymorphisms. Hum Mutat. 2003; 21(6): 557-568.
2. Schaaf MJ, Cidlowski A. Molecular mechanisms of glucocorticoid action and resistance. J Steroid BiochemMol Biol. 2003; 83(1): 37-48.
3. de Castro M, Elliot S, Kino T, et al. The non-ligand binding beta-isoform of the human glucocorticoid receptor (hGR beta) tissue levels, mechanism of action, and potential physiologic role. Mol Med. 1996; 2(5): 597-607.
4. Hamid QA, Wenzel SE, Hauk PJ, et al. Increased glucocorticoid receptor beta in airway cells of glucocorticoid-insensitive asthma. Am J Respir Crit Care Med. 1999; 159(5 Pt 1): 1600-1604.
5. Honda M, Orii F, Ayabe T, et al. Expression of glucocorticoid receptor beta in lymphocytes of patients with glucocorticoid-resistant ulcerative colitis. Gastroenterology. 2000; 118(5): 859-866.
6. Chikanza C. Mechanisms of glucocorticoid resistance in rheumatoid arthritis: a putative role for the corticosteroid receptor beta isoform. Ann N Y Acad Sci, 2002; 966(6): 39-48.
7.张星虎,许贤豪,殷剑,等.重症肌无力患者糖皮质激素受体检测的临床价值.中华内科杂志. 2002; 41(5): 322-324.
8. Webster JC, Oakley RH, Jewell CM, et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance. Proc Natl Acad Sci. 2001; 98(12): 6865-6870.
9.何庆南,易著文,何小解,等. GRβ在肾病综合征患儿中的表达及影响因素研究.中国病理生理杂志. 2002; 18(9): 1042-1045.
10. Oakley RH, Jewell CM, Yudt MR, et al. The dominant negative activity of the human glucocorticoid receptor beta isoform: Specificity and mechanisms of action. J Biol Chem. 1999, 274(39): 27857-27866.
11. Hauk PJ, Hamid QA, Chrousos GP, et al. Induction of corticosteroid insensitivity inhuman PBMCs by microbial superantigens. Allergy Clin Immunol. 2000; 105(4): 782-787.
12. Lu N, Cidlowski J. The origin and functions of multiple human glucocorticoid receptor isoforms. Ann N Y Acad Sci. 2004; 1024(6): 102-123.
1. Minguet S, Huber M, Rosenkranz L. Adenosine and cAMP are potent inhibitors of the NF- kappa B pathway downstream of immunoreceptors. Eur J Immunol. 2005; 35(1): 25-30.
2. Zhang Q, Li PH. Research advances on relationship between nudear factor- kB and glaucoma. Int J Ophthalmo. 2006; 6(4): 840- 843.
3. Hiscott J, Kwon H, Genin P. Hostile takeovers: viral appropriation of the NF-κB pathway. J Clin Invest. 2001; 107(2): 143-151.
4. Danning CL, Illei GG, Hitchon C, et al. Macrophage-derived cytokine and nuclear factor kappaB p65 expression in synovial membrane and skin of patients with psoriatic arthritis. Arthritis Rheum. 2000; 43(6): 1244-1256.
5.杨政,文海泉.寻常型银屑病患者皮肤中诱生型一氧化氮合酶、核因子-κBp65表达及其临床意义.中华皮肤科杂志. 2001; 34(2): 103-104.
6. Burgos P, Metz C, Bull P, et al. Increased expression of c-re1. From the NF-kappaB/Rel family, in T cells from patients with systemic lupus erythematosus. J Rheumatol. 2000; 27 (1): 116-127.
7. Wong HK, Kammer GM, Dennis G, et al. Abnormal NF-kappa B activity in T lymphocytes from patients with systemic lupus erythematosus is associated with decreased p65-RelA protein expression. J Immunol. 1999; 163(3): 1682-1689.
8.许韩师,叶任高,孙林.系统性红斑狼疮患者外周血单一核细胞NF-κB信号通路活化检测.中华皮肤科杂志. 2001; 34(1): 18-21.
9. Li Q, Verma IM. NF-κB regulation in the immune system. Nat Rev Immunol. 2002; 2 (10): 725-734.
10. Qin JZ, Chaturvedi V, Denning MF, et al. Role of NF-κB in the apoptotic-resistant phenotype of keratinocyte. J Biol Chem. 1999; 274(53): 37957-37964.
11. Seitz CS, Freiberg RA, Hinata K, et al. NF-κB determines localization and features of cell death in epidermis. J Clin Invest. 2000; 105(3): 253-260.
12. Auphan N, DiDonato JA, Rosette C, et al. Immunosuppression by glucocorticoids: inhibition of NF-κB activity through induction of IκB synthesis. Science. 1995; 270 (5234): 286-290.
1. Krunkosky TM, Fischer BM, Martin LD, et al. Effects of TNF-alpha on expression of ICAM-1 in human airway epithelial cells in vitro. Signaling pathways controlling surface and gene expression. Am J Respir Cell Mol Biol. 2000; 22 (6): 685-692.
2.冯信忠,陆毅, Corrine L, et al.细胞因子在银屑病非皮损成纤维细胞中的表达.中华皮肤科杂志. 2003; 36 (3): 133-135.
3.王万卷,陈丽,王晓鹏.寻常型银屑病皮损中肿瘤坏死因子-α、基质金属蛋白酶9及其抑制剂-1的表达.西安交通大学学报(医学版). 2007; 28(3): 322-324.
4. Groves RW, Allen MH, Ross EL, et al. Tumor necrosis factor alpha is pro-inflammtary in normal human skin and modulates cutaneous adhesion molecule expression. Br J Dermatol. 1995; 132(3): 345-352.
5. Sheu MY, Fowler AJ, Kao J, et al. Topical peroxisome proliferators activated receptor-alpha activators reduce inflammation in irritant and allergic contant dermatitis models. J Invest Dermatol. 2002; 118(1): 94-101.
6.周伟,张建国,栗超跃. TNF-α诱导脑胶质瘤细胞凋亡过程中NF-κB、IκBα活性的研究.山东医药. 2006, 46(15): 3-4.
7. Yudt MR, Jewell CM, Bienstock RJ, et al. Molecular origins for the dominant negative function of human glucocorticoid receptor beta. Mol Cell Biol. 2003; 23(12): 4319-4330.
8. Kino T, Chrousos GP. Tumor necrosis factor alpha receptor- and Fas-associated FLASH inhibit transcriptional activity of the glucocorticoid receptor by binding to and interfering with its interaction with p160 type nuclear receptor coactivators. J Biol Chem. 2003; 278(5): 3023-3029.
9. Schaaf MJ, Cidlowski JA. AUUUA motifs in the 3, UTA of human glucocorticoid receptor alpha and beta mRNA destabilize mRNA and decrease receptor protein expression. Steroids. 2002; 67(6): 627-636.
10. Leung DY, de Castro M, Szefler SJ, et al. Mechanisms of glucocorticoid resistant asthma. Ann N Y Acad Sci. 1998; 840(6): 735-746.
11. Yudt MR, Jewell CM, Bienstock RJ, et al. Molecular origins for the dominant negative function of human glucocorticoid receptor beta. Mol Cell Biol. 2003; 23 (12): 4319-4330.
12. Pujols L, Mullol J, Picado C. Alpha and beta glucocorticoid receptors: relevance in airway diseases. Curr Allergy Asthma Rep. 2007; 7(2): 93-99.
13. Lewis-Tuffin LJ, Cidlowski JA. The physiology of human glucocorticoid receptor beta (hGRbeta) and glucocorticoid resistance. Ann N Y Acad Sci. 2006; 1069(6): 1-9.
14. Schaaf MJ, Cidlowski JA. Molecular mechanisms of glucocorticoid action and resistance. J Steroid BiochemMol Biol. 2003; 83(1): 37-48.
1.冯信忠,陆毅, Corrine L, et al.细胞因子在银屑病非皮损成纤维细胞中的表达.中华皮肤科杂志. 2003; 36 (3): 133-135.
2.王万卷,陈丽,王晓鹏.寻常型银屑病皮损中肿瘤坏死因子-α、基质金属蛋白酶9及其抑制剂-1的表达.西安交通大学学报(医学版). 2007; 28(3): 322-324.
3. Groves RW, Allen MH, Ross EL, et al. Tumor necrosis factor alpha is pro-inflammtary in normal human skin and modulates cutaneous adhesion molecule expression. Br J Dermatol. 1995; 132(3): 345-352.
4. Sheu MY, Fowler AJ, Kao J, et al. Topical peroxisome proliferators activated receptor-alpha activators reduce inflammation in irritant and allergic contant dermatitis models. J Invest Dermatol. 2002; 118(1): 94-101.
5. Ghosh S, Karin M. Missing pieces in the NF-κB puzzle. Cell. 2002; 109(Suppl): s81- s96.
6. Westergaard M, Henningsen J, Johansen C, et al. Expression and localization of peroxisome proliferators-activated receptors and nuclear factor-kappaB in BoFmal and lesional psoriatic skin. J Invest Dermatol. 2003; 121(5): 1104-1117.
7. Monici MC, Agu ennouz M, Mazzeo A, et al. Activation of nuclear factor-kappaB in inflammatory,myopathies and Duchenne muscular dystrophy. Neurology. 2003; 60(6): 993-997.
8.宋艳丽,文海泉,肖嵘,等.卡介苗多糖核酸调节特应性皮炎患者PBMC中NF-kB和Th1/Th2细胞因子的表达.中华皮肤科杂志. 2007; 40(1): 42-44.
9. Rhodus NL, Cheng B, Myers S, et al. The feasibility of monitoring NF-kappaB associated cytokines: TNF-alpha, IL-1alpha, IL-6, and IL-8 in whole saliva for the malignant transformation of oral lichen planus. Mol Carcinog. 2005; 44(2): 77-82.
10. Rhodus NL, Cheng B, Bowles W, et al. Proinflammatory cytokine levels in saliva before and after treatment of (erosive) oral lichen planus with dexamethasone. Oral Dis. 2006; 12(2): 112-116.
11. Murphy JE, Rebort C, Kupper TS. Interleukin-1 and cutaneous inflammation: a crucial ling between innate and acquired immunity. J Invest Dermatol. 2000; 114(3): 602-608.
12. Robort C, Kupper TS. Inflammatory skin diseases, T cell, and immunsurveillance. NEngl J Med. 1999; 341(24): 1817-1828.
13. Li Q, Verma IM. NF–κB regulation in the immune system. Nat Rve Immunol. 2002; 2(10): 725-734.
1. Irusen E, Matthews JG, Takahashi A, et al. p38 Mitogen-activated protein kinase-induced glucocorticoid receptor phosphorylation reduces its activity: role in steroid-insensitive asthma. J Allergy Clin Immunol. 2002, 109(4): 649-657.
2. Adcock IM, Caramori G. Cross-talk between pro-inflammatory transcription factors and glucocorticoids. Immunol Cell Biol. 2001, 79(4): 376-384.
3. Mathieu M, Gougat C, Jaffuel D, et al. The glucocorticoid receptor gene as a candidate for gene therapy in asthma. Gene Ther. 1999, 6(2): 245-252.
4. Xu Q, Leung DY, Kisich KO. Serine-arginine-rich protein p30 directs alternative splicing of glucocorticoid receptor pre-mRNA to glucocorticoid receptor beta in neutrophils. J Biol Chem. 2003, 278(29): 27112-27118.
5. Savory JG, Préfontaine GG, Lamprechtetal C, et al. Glucocorticoid Receptor Homodimers and Glucocorticoid-Mineralocorticoid Receptor Heterodimers Form in the Cytoplasm through Alternative Dimerization Interfaces. Mol Cell Biol. 2001, 21(3): 781-793.
6. Schaaf MJ, Cidlowski JA. AUUUA motifs in the 3′UTR of human glucocorticoid receptor alpha and beta mRNA destabilize mRNA and decrease receptor protein expression. Steroids. 2002, 67(7): 627-636.
7. Pujols L, Mullol J, Roca Ferrer J, et al. Expressi on of glucocorticoid receptor alpha and beta isoforms in human cells and tissues. Am J Physiol Cell Physiol. 2002, 283(4): C1324-1331.
8. Gougat C, Jaffuel D, Gagliardo R, et al. Overexpression of the human glucocorticoid receptor alpha and beta isoforms inhibits AP-1 and NF-kappaB activities hormone independently. J Mol Med. 2002, 80(5): 309-318.
9. Breslin MB, Geng CD, Vedeckis WV. Multiple promoters exist in the human GR gene, one of which is activated by glucocorticoids. Mol Endocrinol. 2001, 15 (8): 1381-1395.
10. Schottelius A, Wedel S, Weltrich R, et al. Higher expression of glucocorticoid receptor in peripheral mononuclear cells in inflammatory bowel disease. Am J Gast roenterol. 2000, 95(8): 1994-1999.
11. Webster JC, Oakley RH, Jewell CM, et al. Proinflammatory cytokines regulate human glucocorticoid receptor gene expression and lead to the accumulation of the dominant negative beta isoform: a mechanism for the generation of glucocorticoid resistance. Proc Natl Acad Sci USA. 2001, 98(12): 6865-6870.
12. Cho YJ, Lee KE. Decreased glucocorticoid binding affinity to glucocorticoid receptor is important in the poor response to steroid therapy of older-aged patients with severe bronchial asthma. Allergy Asthma Proc. 2003, 24(5): 353-358.
13. Pujols L, Xaubet A, Ramirez J, et al. Expression of glucocorticoid receptors alpha and beta in steroid sensitive and steroid insensitive interstitial lung diseases. Thorax. 2004, 59(8): 687-693.
14. Oakley RH, Jewell CM, Yudt MR, et al. The dominant negative activity of the human glucocorticoid receptor beta isoform. Specificity and mechanisms of action. J Biol Chem. 1999, 274(39): 27857-27866.
15. Sousa AR, Lane SJ, Cidlowski JA, et al. Glucocorticoid resistance in asthma is associated with elevated in vivo expression of the glucocorticoid receptor beta-isoform. J Allergy Clin Immunol. 2000, 105(5): 943-950.
16. Honda M, Orii F, Ayabe T, et al. Expression of glucocorticoid receptor beta in lymphocytes of patients with glucocorticoid-resistant ulcerative colitis. Gastroenterology. 2000, 118(5): 859-866.
17. Chikanza IC. Mechanisms of corticosteroid resistance in rheumatoid arthritis: a putative role for the corticosteroid receptor beta isoform. Ann N Y Acad Sci. 2002, 966(7): 39-48.
18. Gagliardo R, Chanez P, Vignola AM, et al. Glucocorticoid receptor alpha and beta in glucocorticoid dependent asthma. Am J Respir Crit Care Med. 2000, 162(1): 7-13.
19. Goebels N, Michaelis D, Engelhardt M, et al. Diferential expression of perform in muscle infiltrating T cells in polymyositis and dermatomyositis. J Clin Invest. 1996, 97(12): 2905-2910.
20. El-Naghy M, Johnson BH, Chen H, et al. The pathway of leukemic cell death caused by glucocorticoid receptor fragment 465*. Exp Cell Res. 2001, 270(2): 165-175.
21. Chikanza IC. Mechanisms of corticosteroid resistance in rheumtoid arthritis: a putative role for the corticosteroid receptor beta isoform. Ann NY Acad Sci. 2002, 966(7): 39-48.
22.赵玉华,刘秉文.核因子-κB糖皮质激素受体途径的拮抗作用.生理科学进展. 2003,33(3): 261-264.
23. Efthimiou P, Schwartzman S, Kagen LJ. Possible role for tumour necrosis factor inhibitors in the treatment of resistant dermatomyositis and polymyositis: a retrospective study of eight patients. Ann Rheum Dis. 2006, 65(9): 1233-1236.
24. Ramanan AV, Campbell-Webster N, Ota S, et al. The effectiveness of treating juvenile dermatomyositis with methotrexate and aggressively tapered corticosteroids. Arthritis Rheum. 2005, 52(11): 3570-3578.
25. Edge JC, Outland JD, Dempsey JR, et al. Mycopheno1ate mofetil as an effective corticosteroid-sparing therapy for recalcitrant dermatomyositis. Arch Dermatol. 2006, 142(1): 65-69.
26.陈向芳,林炜栋,张汝芝,等.多发性肌炎/皮肌炎患者糖皮质激素受体与微量元素的改变及意义.第二军医大学学报. 2007, 28(7): 793-795.
27. De Bleecker JL, De Paepe B, Vervaet VL, et al. Distribution of glucocorticoid receptor alpha and beta subtypes in the idiopathic inflammatory myopathies. Neuromuscul Disord. 2007, 17(2): 186-193.
28. Stuerenburg HJ, Kunze K. Glucocorticoid receptor concentrations in muscle biopsies from patients with neuromuscular diseases. Eur J Neurol. 1999, 6(4): 469-472.
29. Bamberger CM, Bamberger AM, De Castro M, et al. Glucocorticoid receptorβ, a potential endogenous inhibitor of glucocorticoid action in humans. J Clin Invest. 1995, 95(6): 2435-2441.
30. Goebels N, Michaelis D, Engelhardt M, et al. Differential expression of perforin in muscle-infiltrating T cells in polymyositis and dermatomyositis. J Clin Invest. 1996, 97(12): 2905-2910.
31.刘继峰,李久宏,翟宁,等.多发性肌炎/皮肌炎患者外周血单一核细胞中糖皮质激素受体及热休克蛋白90 mRNA的表达.中华皮肤科杂志. 2004, 37(1): 52.
32.刘继峰,许爱娥,宋芳吉,等.多发性肌炎/皮肌炎患者外周血单个核细胞中糖皮质激素受体α、βmRNA表达与糖皮质激素疗效相关性的研究.中国免疫学杂志. 2007, 23(4): 364-367.
33.宋亮年.甾体激素受体家族.见:卢建,余应年,徐仁宝,主编.受体信号转导系统与疾病.济南:山东科学技术出版社, 1999, 370-381.
34. Wilkens T, De Rijk R. Glucocorticoids and immune function: unknown dimensions andnew frontiers. Immunology Today. 1997, 18(9): 418-412.
35. Miller AH, Spencer RL, Pearce BD, et al. Glucocorticoid receptors are differentially expressed in the cells and tissues of the immune system. Cell Immuno. 1998, 186(1): 45-54.
36.梅冰,康舟军,杨瑞和,等.创伤性休克大鼠中性粒细胞CD18和糖皮质激素受体的变化及纳络酮的治疗作用.中国危重病急救医学. 1999, 11(6): 364-367.
37.林海,肖素芳,林忠清,等.糖皮质激素受体减少对严重烫伤大鼠体内炎症介质水平的影响.中国病理生理杂志. 2000, 16(1): 60-62.
38.李志军,余裕民,李兴福,等.系统性红斑狼疮患者外周血白细胞糖皮质激素受体结合量测定的临床意义.中华风湿病学杂志. 2005, 9(10): 597-600.
39.李久宏,高奎斌,韩秀萍,等.狼疮性肾炎患者外周血单个核细胞中糖皮质激素受体和热休克蛋白90 mRNA表达的研究.中华微生物学和免疫学杂志. 2003, 23(9): 727.
40.李秀,张凤山,李英楠.糖皮质激素受体α在系统性红斑狼疮发病机制中的作用研究.中华风湿病学杂志. 2006, 10(5): 290-293.
41.李久宏,李波,毕桂姣.系统性红斑狼疮患者糖皮质激素及受体mRNA相关性研究.中华皮肤科杂志. 2004, 37(1): 48-49.
42. Jiang T, Liu S, Tan M, et al. The phase-shift mutation in the glucocorticoid receptor gene: potential etiologic significance of neuroendocrine mechanisms in lupus nephritis. Clin Chim Acta. 2001, 313(1-2): 113-117.
43. Ginsberg ZH. Psychophysiological aspects of psoriasis. Dermatol Clin. 1995, 13 (5): 793-803.
44.杨雪琴,彭德河,许传珊,等.银屑病患者的性格及情感分析.中华皮肤科杂志. 1991, 24 (1): 33-34.
45.徐仁宝.休克时糖皮质激素受体的变化及大剂量糖皮质激素抗休克治疗的受体机制.基础医学与临床. 1998, 18(1): 5-10.
46. Weigl BA. Immuno regulatory mechanism and stress hormones in psoriasis. Int J Dermatol. 1998, 37(3): 350-357.
47.樊建勇,杨雪琴,张力军,等.银屑病患者血中糖皮质激素及其受体mRNA的测定及其意义.第四军医大学学报. 2001, 22 (22): 2091-2093.
48.韩良辅,肖华胜,陈景藻.次声作用引起大鼠下丘脑c-fos mRNA与CRF mRNA的表达.第四军医大学学报. 1999, 20(1): 1-3.
49. Karalis K, Sano H, Redwine J, et al. Autocrine or paracrine inflammatory actions of CRH in vivo. Science. 1991, 254 (5): 421-423.
50. Gunduz K, Ozturk G, Terzioglu E, et al. T cell subpopulations and IL-2R in vitiligo. J Dermato1. 2004, 31(2): 94-97.
51. Steitz J, Bruck J, Lenz J, et al. Peripheral CD8+ T cell tolerance against melanocytic self-antigens in the skin is regulated in two steps by CD4+ T cells and local inflammation: mplications for the pathophysiology of vitiligo. J Invest Dermatol. 2005, 124 (1): 144-150.
52. Mandelcom-Monson RL, Shear NH, Yau E, et al. Cytotoxic T lymphocyte reactivity to gpl00, MelanA/MART-1, and tyrosinase, in HLA-A2-positive vitiligo patients. J Invest Dermatol. 2003, 121(3): 550-556.
53. Kroll TM, Bommiasamy H, Boissy RE, et al. 4-Tertiary butyl phenol exposure sensitizes human melanocytes to dendritic cell-mediated killing: relevance to vitiligo. J Invest Dermatol. 2005, 124(4): 798-806.
54. Daneshpazhooh M, Mostofizadeh GM, Behjati J, et al. Anti-thyroid peroxidase antibody and vitiligo: a controlled study. BMC Dermatol. 2006, 6:3.
55. Blomhof A, Kemp EH, Gawkrodger DJ, et al. CTLA4 polymorphisms are associated with vitiligo, in patients with concomitant autoimmune diseases. Pigment Cell Res. 2005, 18(1): 55-58.
56.许清玉,卢念祖,韩建德.糖皮质激素受体在白癜风患者外周血单核细胞中的表达.临床皮肤科杂志. 2007, 36(8): 491-492.
1. Hiscott J, Kwon H, Genin P. Hostile takeovers: viral appropriation of the NF-κB pathway. J Clin Invest. 2001, 107(2): 143-151.
2. Viatour P, Merville MP, Bours V, et al. Phosphorylation of NF-kappa B and I kappa B protein: implications in cancer and inflammation. Trends Biochem Sci. 2005, 30(1): 43-52.
3. Huguet C, Crepieux P, Laudet V. Rel/NF-κB transcription factors and IκB inhibtors: evolution from a unique common ancestor. Oncogene. 1997, 15(24): 2965-2974.
4. Simeonidis S, Stauber D, Chen GY, et al. Mechanisms by which IκB proteins control NF-κB activity. Biochemistry. 1999, 96(1): 49-54.
5. Whiteside ST, Israel A. IκB proteins: structure, function and regulation. Cancer Biol. 1997, 8(2): 75-82.
6. May MJ, Ghosh S. Rel/NF-κB and IκB proteins: an overview. Cancer Biol. 1997, 8(2): 63-73.
7. Chang NS. The non-ankyrin C terminus of IκBαphysically interacts with p53 in vivo and dissociates in response to apoptotic stress, hypoxia, DNA damage, and transforming growth factor-β1-mediated growth suppression. J Biol Chem. 2002, 277(12): 10323-10331.
8. Takaesu G, Surabhi RM, Park KJ, et al. TAK1 is critical for I kappa B kinase-mediated activation of the NF-kappa B pathway. J Mol Biol. 2003, 326 (1): 105-115.
9. Yamazaki S, Muta T, Takeshige K. A novel IκB protein, IκB-zeta, induced by proinflammatory stimuli, negatively regulates nuclear factor-κB in the nuclei. J Biol Chem. 2001, 276(29): 27657-27662.
10. Karin M, Delhase M. The I kappa B kinase (IκK) and NF-kappa B: key elements of proinflammatory signalling. Semin Immunol. 2000, 12(1): 85-98.
11. Yang F, Tang E, Guan K, et al. Iκk beta plays an essential role in the phosphorylation of ReLA/p65 on serine 536 induced by lipopolysaccharide. Immunol. 2003, 170(11): 5630-5635.
12. Li Q, Verma IM. NF–κB regulation in the immune system. Nat Rve Immunol. 2002,2(10): 725-734.
13. Bell S, Degitz K, QuirlingM, et al. Involvement of NF-kappacB signalling in skin physiology and disease. Cell Signal. 2003, 15(1):1-7.
14. Robert C, Kupper TS. Inflammatory skin diseases, T cells, and immune surveillance. N Engl J Med. 1999, 341(24): 1817-1828.
15.郁博,陈德宇,何威.与银屑病发病相关的某些细胞因子.中国麻风皮肤病杂志. 2007, 23(8): 696-698.
16. Danning CL, Illei GG, Hitchon C, et al. Macrophage-derived cytokine and nuclear factor kappaB p65 expression in synovial membrane and skin of patients with psoriatic arthritis. Arthritis Rheum. 2000, 43(6): 1244-1256.
17.杨政,文海泉.寻常型银屑病患者皮肤中诱生型一氧化氮合酶、核因子-κBp65表达及其临床意义.中华皮肤科杂志. 2001, 34(2): 103-104.
18. Bos JD, De Rie MA. The pathogenesis of psoriasis: immunological facts and speculations. Immunol Today. 1999, 20(1): 40-46.
19. Baldwin AS. Control of oncogenesis and cancer therapy resistance by the transcription factor NF-kappaB. J Clin Invest. 2001, 107(1): 241-246.
20. Westergaard M, Henningsen J, Johansen C, et al. Expression and localization of peroxisome proliferators-activated receptors and nuclear factor-kappaB in normal and lesional psoriatic skin. J Invest Dermatol. 2003, 121(5): 1104-1117.
21 Zollner TM, Podda M, Picn C. Proteasome inhibition reduces superantigen-mediaed T cell activation and the severity of psoriasis in a SCID-hu model. J Clin Invest. 2002, 109 (5): 671-679.
22 Tak PP, Firestein GS. NF-kappa B: a key role in inflammatory disease. J Clin Invest. 2001, 107(1): 7-11.
23 Kovacich JC, Boyle EM, Morgan EN, et al. Inhibition of the transcriptional activator protein nuclear factor kappa B prevents hemodynamic instability associated with the whole-body inflammatory response syndrome. J Thorac Cardiovasc Surg. 1999, 118(1): 154-162.
24 Becker H, Stengl G, Stein M, et al. Analysis of proteins that interact with the IL-2 regulatory region in patients with rheumatic diseases. Clin Exp Immunol. 1995, 99(3): 325-330.
25 Monici MC, Aguennouz M, Mazzeo A, et al. Activation of nuclear factor-kappa B in inflammatory, myopathies and Duchenne muscular dystrophy. Neurology. 2003, 60(6): 993-997.
26 Burgos P, Metz C, Bull P, et al. Increased expression of c-re1 From the NF-kappaB/Rel family, in T cells from patients with systemic lupus erythematosus. J Rheumatol. 2000, 27(1): 116-127.
27 Wong HK, Kammer GM, Dennis G, et al. Abnormal NF-kappa B activity in T lymphocytes from patients with systemic lupus erythematosus is associated with decreased p65-RelA protein expression. J Immunol. 1999, 163(3): 1682-1689.
28许韩师,叶任高,孙林.系统性红斑狼疮患者外周血单一核细胞NF-κB信号通路活化检测.中华皮肤科杂志. 2001, 34(1): 18-21.
29 Novak N, Valenta R, Bohle B, et al. Fc(epsilon)RI engagement of Langerhans cell-like dendritic cells and inflammatory dendritic epidermal cell-like dendritic cells induces chemotactic signals and different T-cell phenotypes in vitro. J Allergy Clin Immunol. 2004, 113(5): 949-957.
30宋艳丽,文海泉,肖嵘,等.卡介苗多糖核酸调节特应性皮炎患者PBMC中NF-kB和Th1/Th2细胞因子的表达.中华皮肤科杂志. 2007, 40(1): 42-44.
31谢志强,刘玲玲,窦侠,等.特应性皮炎皮损角质形成细胞NF-κB表达及外用他克莫司对其的影响.北京大学学报(医学版). 2004, 36(5): 487-490.
32 Kaburagi Y, Shimada Y, Nagaoka T, et al. Enhanced production of CC-chemokines (RANTES, MCP-1. MIP-l alpha, MIP-l beta, and eotaxin) in patients with atopic dermatitis. Arch Dermatol Res. 2001, 293(7): 350-355.
33 Huber MA, Denk A, Peter RU, et al. The IKK-2/I kappa B alpha/NF-kappa B pathway plays a key role in the regulation of CCR3 and Eotaxin-l in fibroblasts. A critical link to dermatitis in I kappa Bat-Pha-deficient mice. J Biol Chem. 2002, 277(2): 1268-1275
34 Kim JH, Ha IS, Hwang CI, et al. Gene expression profiling of anti-GBM glomerulonephritis model: the role of NF-kappa B in immune complex kidney disease. Kidney Int. 2004, 66(5): 1826-1837.
35 Baouz S, Giron-Michel J, Azzarone B, et al. Lung myofibroblasts as targets of salmeterol and fluticasone propionate: inhibition of alpha-SMA and NF-kappa B. Int Immunol. 2005, 17(11): 473-1481.
36 Yousaf N, Gould DJ, Aganna E, et al. Tumor necrosis factor receptor I from patients with tumor necrosis factor receptor-associated periodic syndrome interacts with wild-type tumor necrosis factor receptor I and induces ligand-independent NF-kappa B activation. Arthritis Rheum. 2005, 52(9): 2906-2916.
37 Kraft S, Novak N, Katoh N, et al. Aggregation of the high-affinity IgE receptor Fc (epsilon) RI on human monocytes and dendritic cells induces NF-kappa B activation. J Invest Dermatol. 2002, 118(5): 830-837.
38 Nakamura H, Aoki M, Tamai K, et al. Prevention and regression of atopic dermatitis by ointment containing NF-kB decoy oligodeoxynucleotides in NC/Nga atopic mouse model. Gene Ther. 2002, 9(18): 1222-1229.
39 Abeyama K, Eng W, Jester JV, et al. A role for NF-kappa B-dependent gene transactivation in sunburn. J Clin Invest. 2000, 105(12): 1751-1759.
40 Djavaheri Mergny M, Gras MP, Mergny JL, et al. UVA-induced decrease ill nuclear factor-kappaB activity in human keratinocytes. Biochem J. 1999, 338(3): 607-613.
41 Gilmore TD. NF-kappa B is required for H-ras oncogene induced abnormal cell proliferation and tumorigenesis. Oncogene, 2000, 19(7): 841-849.
42 Hinz M, Krappmann D, Eichten A, et al. Nuclear factor-kappa B, cancer, and apoptosis. Mol Cell Biol. 2004, 64(4): 2690-2698.
43 Kaltschmidt B, Kaltschmidt C, Hehner SP, et al. An approach to proteomic analysis of human tumors. Oncogene. 2003, 22(49): 3213-3215.
44 Kiernan R, Bres V, Ng RW, et al. Post-activation turn-off of NF-kappa B-dependent transcription is regulated by acetylation of p65. J Biol Chem. 2003, 278(4): 2758–2766.
45 Digicaylioglu M. Erythropoietin-mediated neuroprotection involves cross-talk between Jak-and NF-κB signaling cascades. Nature. 2001, 412(6847): 641–647.
46 Tamatani M, Mitsuda N, Matsuzaki H, et al. A pathway of neuronal apoptosis induced by hypoxia Preoxygenation: roles of nuclear factor-kappa B and Bcl-2. J Neurochem. 2000, 75(2): 683-693.
47 Foo SY, Nolan GP. Genetic approachs in mice to understand NF-kappa B function. Trends Genet. 2003, 18(6): 229-235.
48 Ciana P, Neri A, Cappellini C, et al. Constitutive expression of lymphoma-associated NFKB-2/Ly1-10 proteins is tumorigenic in murine fibroblasts. Oncogene. 1997, 14(15):1805-1810.
49 Dejardin E, Deregowski V, Chepelier M, et al. The nuclear factor-kappa B: a protential therapeutic target for cancers. Oncogene. 2003, 22(49): 2567-2577.
50 Nakayama H, Ikebe T, Beppu M, et al. High expression levels of nuclear factor kappa B, I kappa B kinase alpha and Akt kinase in squamous cell carcinoma of the oral cavity. Cancer. 2001, 92(12): 3037-3044.
51 Budunova IV, Perez P, Vaden VR, et al. Increased expression of p50 NF-kappa B and constitutive activation of NF-kappa B transcription factors during mouse skin carcinogenesis. Oncogene. 1999, 18(52): 7423-7431.
52 Hodgson L, Henderson AJ, Dong C. Melanoma cell migration to type IV collagen requires activation of NF-kappa B. Oncogene. 2003, 22(1): 98-108.
53 Kashani Sabet M, Liu Y, Fong S, et al. Identification of gene function and functional pathways by systetmic plasmid-based ribozyme targeting in adult mice. Proc Natl Acad Sci USA. 2002, 99(6): 3878-3883.
54 Izaban KF, Ergin M, Qin JZ, et al. Constitutive expression of NF-κB is a characteristic feature of mycosis fungoides: implications for apoptosis resistance and pathogenesis. Hum Pathol. 2000, 31(12): 1482-1490.
55王海林,侯建新,周桂芝,等.皮肤淋巴瘤中c-myb和NF-κB的表达及意义.中国麻风皮肤病杂志. 2007, 23(5): 384-387.
56 Aradhya S, Wofiendin H, Jakins T, et al. A recurrent deletion in the ubiquitously expressed NEMO(IKK-gamma) gene accounts for the vast majority of incontinentia pigmenti mutations. Hum Mol Genet. 2001, 10(19): 2171-2179.
57 Smahi A, Courtois G, Rabia SH, et al. The NF-kappa B signaling pathway in human diseases: from incontinentia pigmenti to ectodermal dysplasias and immune-deficiency syndromes. Hum Mol Genet. 2002, 11(20): 2371-2375.
58 Santoro A, Majorana A, Bardellini E, et al. NF-kappa B expression in oral and cutaneous lichen planus. Pathol. 2003, 201(3): 466-472.
59 Rhodus NL, Cheng B, Myers S, et al. The feasibility of monitoring NF-kappa B associated cytokines: TNF-alpha, IL-1alpha, IL-6, and IL-8 in whole saliva for the malignant transformation of oral lichen planus. Mol Carcinog. 2005, 44(2): 77-82.
60 Rhodus NL, Cheng B, Bowles W, et al. Proinflammatory cytokine levels in saliva before and after treatment of (erosive) oral lichen planus with dexamethasone. Oral Dis. 2006, 12(2): 112-116.
61任晓丽,白莉.核因子κB、细胞间黏附分子1在扁平苔藓中的表达和意义.中国麻风皮肤病杂志. 2007, 23(7): 596-598.
© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号 地址：北京市海淀区学院路29号 邮编：100083 电话：办公室：(+86 10)66554848；文献借阅、咨询服务、科技查新：66554700 |