14-3-3gamma对神经元缺氧缺血损伤的保护作用及机制研究
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摘要
[背景]在脑组织中14-3-3蛋白十分丰富。14-3-3gamma主要在神经元表达。我们曾报道14-3-3gamma在体外缺血培养的星形胶质细胞中表达上调，并且通过结合磷酸化Bad减少缺血诱导的胶质细胞死亡。[目的]研究14-3-3蛋白在缺血损伤的神经元中的表达，保护作用和机制。[方法和结果]通过Western blot，免疫荧光染色，免疫共沉淀以及原代神经元核转染等方法，我们发现原代培养的小鼠大脑皮层神经元缺血处理后14-3-3gamma表达明显增加。而14-3-3beta，epsilon，eta和zeta在相同处理下没有明显的变化。过度表达14-3-3特异结合蛋白(Diforpein)导致小鼠神经瘤母细胞(N2a)和原代神经元死亡增加。而过度表达14-3-3gamma显著减少缺血诱导的N2a和原代神经元的死亡。除此之外，我们在培养的N2a和原代神经元中加入特异降解14-3-3gamma的siRNA也增加缺血诱导的细胞死亡。为了明确14-3-3gamma在缺血性损伤中的保护机制，通过免疫共沉淀方法，我们发现在原代培养的小鼠大脑皮层神经元经缺血处理后，14-3-3gamma上调并特异结合同时上调的丝氨酸37位点磷酸化beta-catenin，而它与Ask-1没有明显的相互作用。另外，我们还发现在过度表达14-3-3gamma的N2a细胞中，Bax的表达明显下调；而过度表达降解内源性14-3-3gamma-siRNA，Bax的表达增加。在氯化钴诱导的缺氧预适应动物模型中，动物耐受缺氧存活时间明显延长，14-3-3gamma的表达上调，而其它14-3-3亚型发生不同的变化，Bax和p53的表达没有明显影响。[结论]上述结果表明，在缺血神经元14-3-3gamma表达上调并结合磷酸化beta-catenin，降低Bax的表达发挥减轻缺血神经元损伤的重要内源性保护机制，缺氧预适应导致内源性14-3-3gamma上调增加动物耐受缺氧。
14-3-3 proteins are abundant in brain tissues and the gamma isoform is mainly expressed in neurons. We have previously reported that 14-3-3gamma could be up-regulated in astrocytes by in vitro ischemia and attenuated ischemia-induced astrocytic death by binding to phosphorylated Bad. In this study, we studied the expression, function and underlying mechanism of 14-3-3gamma in ischemic neurons. The selective up-regulation of 14-3-3gamma in primary cultures of mouse cerebral cortical neurons exposed to oxygen-glucose deprivation (OGD) was demonstrated by Western blot analysis, immunostaining and co-immunoprecipitation methods. Other 14-3-3 isoforms (β,ε,ηandζwere not altered significantly by OGD treatment. Blocking the interaction of 14-3-3 proteins with their ligands by over-expression diforpein (DFP) exacerbated cell death in primary mouse cortical neurons and N2a neuroblastoma cells. Over-expression of 14-3-3gamma enhanced cell survival in OGD-treated neurons and N2a cells significantly while other 14-3-3 isoforms were less effective. Moreover, suppressing 14-3-3gamma expression by siRNA technique facilitated cell death in neurons and N2a cells upon OGD treatment. To study the underlying protective mechanism of 14-3-3gamma, we investigated the interaction of 14-3-3gamma with beta-catenin, Bad, p53 and Ask-1. We found that 14-3-3gamma bound more phospho-s37-beta-catenin in neurons upon OGD incubation while the binding of 14-3-3gamma with Bad, p53 and Ask-1 did not altered evidently. In addition, the expression of Bax was reduced in N2a cells overexpressed 14-3-3gamma while 14-3-3gamma-siRNA increased the Bax level in N2a cells. Finally, in the model of anoxia preconditioning induced by cobalt chloride, we found that the expression of 14-3-3 gamma but not other 14-3-3 isoform was increased in cerebral cortex compared with control. Taken together, these data suggested that 14-3-3gamma-beta-catenin-Bax pathway was an important part of endogenous protective machinery in ischemic neurons. The induction of 14-3-3 gamma may be a protective mechanism of preconditioning.
14-3-3 proteins are abundant in brain tissues and the gamma isoform is mainly expressed in neurons. We have previously reported that 14-3-3gamma could be up-regulated in astrocytes by in vitro ischemia and attenuated ischemia-induced astrocytic death by binding to phosphorylated Bad. In this study, we studied the expression, function and underlying mechanism of 14-3-3gamma in ischemic neurons. The selective up-regulation of 14-3-3gamma in primary cultures of mouse cerebral cortical neurons exposed to oxygen-glucose deprivation (OGD) was demonstrated by Western blot analysis, immunostaining and co-immunoprecipitation methods. Other 14-3-3 isoforms (β,ε,ηandζwere not altered significantly by OGD treatment. Blocking the interaction of 14-3-3 proteins with their ligands by over-expression diforpein (DFP) exacerbated cell death in primary mouse cortical neurons and N2a neuroblastoma cells. Over-expression of 14-3-3gamma enhanced cell survival in OGD-treated neurons and N2a cells significantly while other 14-3-3 isoforms were less effective. Moreover, suppressing 14-3-3gamma expression by siRNA technique facilitated cell death in neurons and N2a cells upon OGD treatment. To study the underlying protective mechanism of 14-3-3gamma, we investigated the interaction of 14-3-3gamma with beta-catenin, Bad, p53 and Ask-1. We found that 14-3-3gamma bound more phospho-s37-beta-catenin in neurons upon OGD incubation while the binding of 14-3-3gamma with Bad, p53 and Ask-1 did not altered evidently. In addition, the expression of Bax was reduced in N2a cells overexpressed 14-3-3gamma while 14-3-3gamma-siRNA increased the Bax level in N2a cells. Finally, in the model of anoxia preconditioning induced by cobalt chloride, we found that the expression of 14-3-3 gamma but not other 14-3-3 isoform was increased in cerebral cortex compared with control. Taken together, these data suggested that 14-3-3gamma-beta-catenin-Bax pathway was an important part of endogenous protective machinery in ischemic neurons. The induction of 14-3-3 gamma may be a protective mechanism of preconditioning.
引文
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23. Nurmi SM, Gahmberg CG, Fagerholm SC. 14-3-3 proteins bind both filamin and alphaLbeta2 integrin in activated T cells. Ann N Y Acad Sci. 2006,1090:318-25.
24. Dai JG, Murakami K. Constitutively and autonomously active protein kinase C associated with 14-3-3 zeta in the rodent brain. J Neurochem. 2003, 84(1):23-34.
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28. Tsuruta F, Sunayama J, Mori Y, Hattori S, Shimizu S, Tsujimoto Y, Yoshioka K,Masuyama N, Gotoh Y. JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins. EMBO J. 2004,23(8): 1889-99.
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1.Dong Zhao,Jing Liu,Wei Wang.Epidemiological Transition of Stroke in China.Stroke.2008;39:1668-1674
2.Ming Liu,Bo Wu,Wen-Zhi Wang.The Lancet Neurology.2007,6(5):456-464.
3.Stoll G,Kleinschnitz C,Nieswandt B.Molecular mechanisms of thrombus formation in ischemic stroke:novel insights and targets for treatment.Blood.2008,112(9):3555-62.
4.Moore,B.W.and Perez,V.J.Specific Acid Proteins in theNervous System.Prentice-Hall,1967.
5.Aitken,A.14-3-3 proteins:a historic overview.Semin.Cancer Biol.2006,16,162-172
6.Aitken A,Ellis CA,Harris A,Sellers LA,Toker A.Kinase and neurotransmitters.Nature(London)1990;344:594.
7.Fantl W J,Muslin A J,Kikuchi A,Martin JA,MacNicol AM,Gross RW,et al.Activation of Raf-1 by 14-3-3 proteins.Nature 1994;371:612-4.
8.Fu H,Xia K,Pallas DC,Cui C,Conroy K,Narsimhan RP,et al.Interaction of the protein kinase Raf-1 with 14-3-3 proteins. Science 1994;266:126-9.
9. Yuan Z, Becker EB, Merlo P, Yamada T, Schaefer EM, Bonni A. Activation of FOXO1 by Cdkl in cycling cells and postmitotic neurons. Science. 2008, 319(5870): 1665-8.
10. Brunet A, Bonni A, Juo P, Hu LS, et al. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell 1999;96:857-68.
11. Conklin DS, Galaktionov K, Beach D. 14-3-3 proteins associate with cdc25 phosphatases. Proc Natl Acad Sci USA. 1995;92:7892-6.
12. Obsil T, Ghirlando R, Klein DC, Ganguly S, Dyda F. Crystal structure of the 14-3-3zeta:serotonin N-acetyltransferase complex, a role for scaffolding in enzyme regulation..Cell.2001, 105(2):257-67.
13. Wang AH, Kruhlak MJ, Wu J, Bertos NR, Vezmar M, Posner BI, Bazett-Jones DP, Yang XJ. Regulation of histone deacetylase 4 by binding of 14-3-3 proteins. Mol Cell Biol.2000,20(18):6904-12.
14. Nurmi SM, Gahmberg CG, Fagerholm SC. 14-3-3 proteins bind both filamin and alphaLbeta2 integrin in activated T cells. Ann N Y Acad Sci. 2006; 1090:318-25.
15. Dai JG, Murakami K. Constitutively and autonomously active protein kinase C associated with 14-3-3 zeta in the rodent brain. J Neurochem. 2003, 84(1):23-34.
16. Zha J, Harada H, Yang E, Jockel J, Korsmeyer SJ. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L).Cell. 1996, 87:619-28.
17. Samuel T, Weber HO, Rauch P, Verdoodt B, Eppel JT, McShea A, Hermeking H, Funk JO. The G2/M regulator 14-3-3sigma prevents apoptosis through sequestration of Bax. J Biol Chem. 2001, 276(48):45201-6.
18. Nomura M, Shimizu S, Sugiyama T, Narita M, Ito T, Matsuda H, Tsujimoto Y. 14-3-3 Interacts directly with and negatively regulates pro-apoptotic Bax. J Biol Chem. 2003,278(3):2058-65.
19. Tsuruta F, Sunayama J, Mori Y, Hattori S, Shimizu S, Tsujimoto Y, Yoshioka K, Masuyama N, Gotoh Y. JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins. EMBO J. 2004, 23(8): 1889-99.
20. Gardino, A.K. et al. Structural determinants of 14-3-3 binding specificities and regulation of subcellular localization of 14-3-3-ligand complexes: a comparison of the X-ray crystal structures of all human 14-3-3 isoforms. Semin Cancer Biol. 2006, 16,173-182.
21. Siman R, Roberts VL, McNeil E. Biomarker evidence for mild central nervous system injury after surgically-induced circulation arrest. Brain Res. 2008,1213:1-11.
22. Siman R, Mclntosh TK, Soltesz KM. Proteins released from degenerating neurons are surrogate markers for acute brain damage. Neurobiol Dis. 2004, 16(2):311-20.
23. Yu F, Narasimhan P, Chan PH. Increased expression of a proline-rich Akt substrate (PRAS40) in human copper/zinc-superoxide dismutase transgenic rats protects motor neurons from death after spinal cord injury. J Cereb Blood Flow Metab. 2008,28(1):44-52.
24. Kamada H, Nito C, Endo H, Chan PH. Bad as a converging signaling molecule between survival PI3-K/Akt and death JNK in neurons after transient focal cerebral ischemia in rats. J Cereb Blood Flow Metab. 2007, 27(3):521-33
25. Saito A, Hayashi T, Okuno S, Nishi T, Chan PH. Modulation of proline-rich akt substrate survival signaling pathways by oxidative stress in mouse brains after transient focal cerebral ischemia. Stroke. 2006, 37(2):513-7.
26. Satoh J, Tabunoki H, Nanri Y, Arima K, Yamamura T.Human astrocytes express 14-3-3 sigma in response to oxidative and DNA-damaging stresses. Neurosci Res. 2006,56(1):61-72.
27. Wang XT, Pei DS, Xu J, Guan QH, Sun YF, Liu XM, Zhang GY. Opposing effects of Bad phosphorylation at two distinct sites by Akt1 and JNK 1/2 on ischemic brain injury.Cell Signal. 2007, 19(9): 1844-56.
28. Koh PO. Melatonin prevents the injury-induced decline of Akt/forkhead transcription factors phosphorylation. J Pineal Res. 2008,45(2): 199-203.
29. Koh PO. Melatonin attenuates the focal cerebral ischemic injury by inhibiting the dissociation of pBad from 14-3-3. J Pineal Res. 2008,44(1): 101-6.
30. Chen XQ, Fung YW, Yu AC. Association of 14-3-3gamma and phosphorylated bad attenuates injury in ischemic astrocytes. J Cereb Blood Flow Metab. 2005,25(3):338-47.
31. Chen XQ, Chen JG, Zhang Y, Hsiao WW, Yu AC. 14-3-3gamma is upregulated by in vitro ischemia and binds to protein kinase Raf in primary cultures of astrocytes. Glia.2003,42(4):315-24.
32. Chen XQ, Liu S, Qin LY, Wang CR, Fung YW, Yu AC. Selective regulation of 14-3-3 eta in primary culture of cerebral cortical neurons and astrocytes during development. J Neurosci Res. 2005, 79(1-2): 114-8.
33. Chen XQ, Yu AC. The association of 14-3-3gamma and actin plays a role in cell division and apoptosis in astrocytes. Biochem Biophys Res Commun. 2002,296(3):657-63.
34. Kawamoto Y, Akiguchi I, Tomimoto H, Shirakashi Y, Honjo Y, Budka H. Upregulated expression of 14-3-3 proteins in astrocytes from human cerebrovascular ischemic lesions. Stroke. 2006, 37(3):830-5.
35. Li H, Guo Y, Teng J, Ding M, Yu AC, Chen J. 14-3-3gamma affects dynamics and integrity of glial filaments by binding to phosphorylated GFAP. J Cell Sci. 2006, 119(Pt 21):4452-61.
36. Ye SQ, Lai XJ, Luo ZZ, Li L, Chen XQ (corresponding author). 14-3-3 protects ischemic neurons from apoptosis by transcriptional down-regulating Bax through beta-catenin. 2009, submitted.
37. Wu JS, Cheung WM, Lin TN.Ligand-activated peroxisome proliferator activated receptor-gamma protects against ischemic cerebral infarction and neuronal apoptosis by 14-3-3 epsilon upregulation. Circulation. 2009,119(8): 1124-34.
38. Downey JM, Cohen MV. Signal transduction in ischemic preconditioning. Adv Exp Med Biol. 1997,430:39.
39. Downey JM, Liu GS, Thornton JD. Adenosine and the anti-infarct effects of preconditioning. Cardiovasc Res, 1993, 27:3.
40. Mabanta L, Valane P, Borne J, et al. Initiation of remote microvascular preconditioning requires K(ATP) channel activity. Am J Physiol Heart Circ Physiol 2006, 290:H264.
41. Jiang Z, Zhang Y, Chen XQ, Lam PY, Yang H, Xu Q, Yu AC. Activation of Erk1/2 and Akt in astrocytes under ischemia. Biochem Biophys Res Commun. 2002,294(3):726-33.
42. QG Zhang, et al. Ischemic preconditioning negatively regulates plenty of SH3s-mixed lineage kinase 3-Racl complex and c-Jun N-terminal kinase 3 signaling via activation of Akt. Neuroscience, 2006, 143: 431-444.
43. CW Yang, et al. Ischemic preconditioning suppresses apoptosis of rabbit spinal neurocytes by inhibiting ASK1-14-3-3 dissociation. Neuroscience Letters, 2008, 441:267-271.
44. Shiga Y, Wakabayashi H, Miyazawa K, Kido H, Itoyama Y. 14-3-3 protein levels and isoform patterns in the cerebrospinal fluid of Creutzfeldt-Jakob disease patients in the progressive and terminal stages. J Clin Neurosci. 2006, 13(6):661-5.
45. Umahara T, Uchihara T, Tsuchiya K, Nakamura A, Iwamoto T, Ikeda K, Takasaki M. 14-3-3 proteins and zeta isoform containing neurofibrillary tangles in patients with Alzheimer's disease. Acta Neuropathol. 2004 , 108(4):279-86.
46. Santpere G, Puig B, Ferrer I. Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy. Neuroscience. 2007,146(4): 1640-51.
47. Sato S, Chiba T, Sakata E, Kato K, Mizuno Y, Hattori N, Tanaka K. 14-3-3eta is a novel regulator of parkin ubiquitin ligase. EMBO J. 2006, 25(1):211-21.
2. Shiga Y, Wakabayashi H, Miyazawa K, Kido H, Itoyama Y. 14-3-3 protein levels and isoform patterns in the cerebrospinal fluid of Creutzfeldt-Jakob disease patients in the progressive and terminal stages. J Clin Neurosci. 2006,13(6):661-5.
3. Umahara T, Uchihara T, Tsuchiya K, Nakamura A, Iwamoto T, Ikeda K, Takasaki M.14-3-3 proteins and zeta isoform containing neurofibrillary tangles in patients with Alzheimer's disease. Acta Neuropathol. 2004 ,108(4):279-86.
4. Santpere G, Puig B, Ferrer I. Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy. Neuroscience. 2007,146(4): 1640-51.
5. Sato S, Chiba T, Sakata E, Kato K, Mizuno Y, Hattori N, Tanaka K. 14-3-3eta is a novel regulator of parkin ubiquitin ligase. EMBO J. 2006, 25(1):211-21.
6. Beal, 2000 M.F. Beal, Energetics in the pathogenesis of neurodegenerative diseases,Trends Neurosci 23 (7) (2000), pp. 298-304.
7. Dong Zhao, Jing Liu, Wei Wang. Epidemiological Transition of Stroke in China. Stroke.2008;39:1668-1674
8. Ming Liu, Bo Wu, Wen-Zhi Wang. The Lancet Neurology. 2007, 6(5): 456-464.
9. Downey JM, Cohen MV. Signal transduction in ischemic preconditioning. Adv Exp Med Biol. 1997,430:39.
10. Downey JM, Liu GS, Thornton JD. Adenosine and the anti-infarct effects of preconditioning. Cardiovasc Res, 1993, 27:3.
11. Mabanta L, Valane P, Borne J, et al. Initiation of remote microvascular preconditioning requires K(ATP) channel activity. Am J Physiol Heart Circ Physiol 2006, 290:H264.
12. Jiang Z, Zhang Y, Chen XQ, Lam PY, Yang H, Xu Q, Yu AC. Activation of Erk1/2 and Akt in astrocytes under ischemia. Biochem Biophys Res Commun. 2002,294(3):726-33.
13. Moore, B.W. and Perez, V.J. Specific Acid Proteins in theNervous System. Prentice-Hall, 1967.
14. Aitken, A. 14-3-3 proteins: a historic overview. Semin. Cancer Biol. 2006, 16, 162-172.
15. Aitken A, Ellis CA, Harris A, Sellers LA, Toker A. Kinase and neurotransmitters.Nature (London) 1990;344:594.
16. Fantl WJ, Muslin AJ, Kikuchi A, Martin JA, MacNicol AM, Gross RW, et al. Activation of Raf-1 by 14-3-3 proteins. Nature 1994;371:612-4.
17. Fu H, Xia K, Pallas DC, Cui C, Conroy K, Narsimhan RP, et al. Interaction of the protein kinase Raf-1 with 14-3-3 proteins. Science 1994;266:126-9.
18. Yuan Z, Becker EB, Merlo P, Yamada T, DiBacco S, Konishi Y, Schaefer EM, Bonni A.Activation of FOXOl by Cdkl in cycling cells and postmitotic neurons. Science. 2008,319(5870):1665-8.
19. Brunet A, Bonni A, Zigmond MJ, Lin MZ, Juo P, Hu LS, et al. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell 1999;96:857-68.
20. Conklin DS, Galaktionov K, Beach D. 14-3-3 proteins associate with cdc25 phosphatases. Proc Natl Acad Sci USA. 1995 ;92:7892-6.
21. Obsil T, Ghirlando R, Klein DC, Ganguly S, Dyda F. Crystal structure of the 14-3-3zeta:serotonin N-acetyltransferase complex, a role for scaffolding in enzyme regulation..Cell.2001, 105(2):257-67.
22. Wang AH, Kruhlak MJ, Wu J, Bertos NR, Vezmar M, Posner BI, Bazett-Jones DP, Yang XJ. Regulation of histone deacetylase 4 by binding of 14-3-3 proteins. Mol Cell Biol.2000,20(18):6904-12.
23. Nurmi SM, Gahmberg CG, Fagerholm SC. 14-3-3 proteins bind both filamin and alphaLbeta2 integrin in activated T cells. Ann N Y Acad Sci. 2006,1090:318-25.
24. Dai JG, Murakami K. Constitutively and autonomously active protein kinase C associated with 14-3-3 zeta in the rodent brain. J Neurochem. 2003, 84(1):23-34.
25. Zha J, Harada H, Yang E, Jockel J, Korsmeyer SJ. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L).Cell. 1996, 87:619-28.
26. Samuel T, Weber HO, Rauch P, Verdoodt B, Eppel JT, McShea A, Hermeking H, Funk JO. The G2/M regulator 14-3-3sigma prevents apoptosis through sequestration of Bax. J Biol Chem. 2001, 276(48):45201-6.
27. Nomura M, Shimizu S, Sugiyama T, Narita M, Ito T, Matsuda H, Tsujimoto Y. 14-3-3 Interacts directly with and negatively regulates pro-apoptotic Bax. J Biol Chem. 2003,278(3):2058-65.
28. Tsuruta F, Sunayama J, Mori Y, Hattori S, Shimizu S, Tsujimoto Y, Yoshioka K,Masuyama N, Gotoh Y. JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins. EMBO J. 2004,23(8): 1889-99.
29. Siman R, Roberts VL, McNeil E. Biomarker evidence for mild central nervous system injury after surgically-induced circulation arrest. Brain Res. 2008, 1213:1-11.
30. Siman R, McIntosh TK, Soltesz KM. Proteins released from degenerating neurons are surrogate markers for acute brain damage. Neurobiol Dis. 2004, 16(2):311-20.
31. Yu F, Narasimhan P, Chan PH. Increased expression of a proline-rich Akt substrate (PRAS40) in human copper/zinc-superoxide dismutase transgenic rats protects motor neurons from death after spinal cord injury. J Cereb Blood Flow Metab. 2008,28(1):44-52.
32. Kamada H, Nito C, Endo H, Chan PH. Bad as a converging signaling molecule between survival PI3-K/Akt and death JNK in neurons after transient focal cerebral ischemia in rats. J Cereb Blood Flow Metab. 2007, 27(3):521-33
33. Saito A, Hayashi T, Okuno S, Nishi T, Chan PH. Modulation of proline-rich akt substrate survival signaling pathways by oxidative stress in mouse brains after transient focal cerebral ischemia. Stroke. 2006, 37(2):513-7.
34. Wang XT, Pei DS, Xu J, Guan QH, Sun YF, Liu XM, Zhang GY. Opposing effects of Bad phosphorylation at two distinct sites by Aktl and JNK1/2 on ischemic brain injury.Cell Signal. 2007, 19(9): 1844-56.
35. Koh PO. Melatonin prevents the injury-induced decline of Akt/forkhead transcription factors phosphorylation. J Pineal Res. 2008,45(2):199-203.
36. Koh PO. Melatonin attenuates the focal cerebral ischemic injury by inhibiting the dissociation of pBad from 14-3-3. J Pineal Res. 2008,44(1):101-6.
37. Chen XQ, Fung YW, Yu AC. Association of 14-3-3gamma and phosphorylated bad attenuates injury in ischemic astrocytes. J Cereb Blood Flow Metab. 2005,25(3):338-47.
38. Chen XQ, Chen JG, Zhang Y, Hsiao WW, Yu AC. 14-3-3gamma is upregulated by in vitro ischemia and binds to protein kinase Raf in primary cultures of astrocytes. Glia.2003,42(4):315-24.
39. Chen XQ, Liu S, Qin LY, Wang CR, Fung YW, Yu AC. Selective regulation of 14-3-3eta in primary culture of cerebral cortical neurons and astrocytes during development. J Neurosci Res. 2005, 79(1-2):114-8.
40. Chen XQ, Yu AC. The association of 14-3-3gamma and actin plays a role in cell division and apoptosis in astrocytes. Biochem Biophys Res Commun. 2002,296(3):657-63.
41. Deborah K. M. The 14-3-3 proteins: integrators of diverse signaling cues that impact cell fate and cancer development. Trends in Cell Biology. 2008, 19(1): 16-23
42. Kawamoto Y, Akiguchi I, Tomimoto H.Upregulated expression of 14-3-3 proteins in astrocytes from human cerebrovascular ischemic lesions. Stroke. 2006, 37(3):830-5.
43. Satoh J, Tabunoki H, Nanri Y, Arima K, Yamamura T. Human astrocytes express 14-3-3 sigma in response to oxidative and DNA-damaging stresses. Neurosci Res. 2006, 56(1):61-72.
44. Wu JS, Cheung WM, Tsai YS, Chen YT, Fong WH, Tsai HD, Chen YC, Liou JY, Shyue SK, Chen JJ, Chen YE, Maeda N, Wu KK, Lin TN. Ligand-activated peroxisome proliferator-activated receptor-gamma protects against ischemic cerebral infarction and neuronal apoptosis by 14-3-3 epsilon upregulation. Circulation. 2009, 119(8): 1124-34.
45. Kamada H, Nito C, Endo H, Chan PH. Bad as a converging signaling molecule between survival PI3-K/Akt and death JNK in neurons after transient focal cerebral ischemia in rats. J Cereb Blood Flow Metab. 2007,27(3):521-33.
46. Pei DS, Wang XT, Liu Y, Sun YF, Guan QH, Wang W, Yan JZ, Zong YY, Xu TL, Zhang GY. Neuroprotection against ischaemic brain injury by a GluR6-9c peptide containing the TAT protein transduction sequence. Brain. 2006,129(Pt 2):465-79.
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48. Li FQ, Mofunanya A, Harris K, Takemaru K. Chibby cooperates with 14-3-3 to regulate beta-catenin subcellular distribution and signaling activity. J Cell Biol. 2008,
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50. Heusser K, Yuan H, Neagoe I, Tarasov AI, Ashcroft FM, Schwappach B. Scavenging of 14-3-3 proteins reveals their involvement in the cell-surface transport of ATP-sensitive K+ channels. J Cell Sci. 2006, 119(Pt 20):4353-63.
51. Li Y, Wu Y, Li R, Zhou Y. The role of 14-3-3 dimerization in its modulation of the CaV2.2 channel. Channels (Austin). 2007, 1(1): 1-2.
52. Liang X, Butterworth MB, Peters KW, Walker WH, Frizzell RA. An obligatory heterodimer of 14-3-3beta and 14-3-3epsilon is required for aldosterone regulation of the epithelial sodium channel. J Biol Chem. 2008,283(41):27418-25.
53. Nielsen MD, Luo X, Biteau B, Syverson K, Jasper H. 14-3-3 Epsilon antagonizes FoxO to control growth, apoptosis and longevity in Drosophila. Aging Cell. 2008,7(5):688-99.
54. Komiya Y, Kurabe N, Katagiri K, Ogawa M, Sugiyama A, Kawasaki Y, Tashiro F. A novel binding factor of 14-3-3beta functions as a transcriptional repressor and promotes anchorage-independent growth, tumorigenicity, and metastasis. J Biol Chem. 2008,283(27): 18753-64.
55. Liu HM, Li JX, Chen LB. Ischemic preconditioning relieves ischemia/reperfusion injury of hippocampus neurons in rat by inhibiting p53 and bax expressions. Chin Med Sci J. 2007, 22(2): 123-7.
56. QG Zhang, et al. Ischemic preconditioning negatively regulates plenty of SH3s-mixed lineage kinase 3-Rac1 complex and c-Jun N-terminal kinase 3 signaling via activation of Akt. Neuroscience, 2006, 143: 431-444.
57. CW Yang, et al. Ischemic preconditioning suppresses apoptosis of rabbit spinal neurocytes by inhibiting ASK1-14-3-3 dissociation. Neuroscience Letters, 2008, 441:267-271.
1.Dong Zhao,Jing Liu,Wei Wang.Epidemiological Transition of Stroke in China.Stroke.2008;39:1668-1674
2.Ming Liu,Bo Wu,Wen-Zhi Wang.The Lancet Neurology.2007,6(5):456-464.
3.Stoll G,Kleinschnitz C,Nieswandt B.Molecular mechanisms of thrombus formation in ischemic stroke:novel insights and targets for treatment.Blood.2008,112(9):3555-62.
4.Moore,B.W.and Perez,V.J.Specific Acid Proteins in theNervous System.Prentice-Hall,1967.
5.Aitken,A.14-3-3 proteins:a historic overview.Semin.Cancer Biol.2006,16,162-172
6.Aitken A,Ellis CA,Harris A,Sellers LA,Toker A.Kinase and neurotransmitters.Nature(London)1990;344:594.
7.Fantl W J,Muslin A J,Kikuchi A,Martin JA,MacNicol AM,Gross RW,et al.Activation of Raf-1 by 14-3-3 proteins.Nature 1994;371:612-4.
8.Fu H,Xia K,Pallas DC,Cui C,Conroy K,Narsimhan RP,et al.Interaction of the protein kinase Raf-1 with 14-3-3 proteins. Science 1994;266:126-9.
9. Yuan Z, Becker EB, Merlo P, Yamada T, Schaefer EM, Bonni A. Activation of FOXO1 by Cdkl in cycling cells and postmitotic neurons. Science. 2008, 319(5870): 1665-8.
10. Brunet A, Bonni A, Juo P, Hu LS, et al. Akt promotes cell survival by phosphorylating and inhibiting a Forkhead transcription factor. Cell 1999;96:857-68.
11. Conklin DS, Galaktionov K, Beach D. 14-3-3 proteins associate with cdc25 phosphatases. Proc Natl Acad Sci USA. 1995;92:7892-6.
12. Obsil T, Ghirlando R, Klein DC, Ganguly S, Dyda F. Crystal structure of the 14-3-3zeta:serotonin N-acetyltransferase complex, a role for scaffolding in enzyme regulation..Cell.2001, 105(2):257-67.
13. Wang AH, Kruhlak MJ, Wu J, Bertos NR, Vezmar M, Posner BI, Bazett-Jones DP, Yang XJ. Regulation of histone deacetylase 4 by binding of 14-3-3 proteins. Mol Cell Biol.2000,20(18):6904-12.
14. Nurmi SM, Gahmberg CG, Fagerholm SC. 14-3-3 proteins bind both filamin and alphaLbeta2 integrin in activated T cells. Ann N Y Acad Sci. 2006; 1090:318-25.
15. Dai JG, Murakami K. Constitutively and autonomously active protein kinase C associated with 14-3-3 zeta in the rodent brain. J Neurochem. 2003, 84(1):23-34.
16. Zha J, Harada H, Yang E, Jockel J, Korsmeyer SJ. Serine phosphorylation of death agonist BAD in response to survival factor results in binding to 14-3-3 not BCL-X(L).Cell. 1996, 87:619-28.
17. Samuel T, Weber HO, Rauch P, Verdoodt B, Eppel JT, McShea A, Hermeking H, Funk JO. The G2/M regulator 14-3-3sigma prevents apoptosis through sequestration of Bax. J Biol Chem. 2001, 276(48):45201-6.
18. Nomura M, Shimizu S, Sugiyama T, Narita M, Ito T, Matsuda H, Tsujimoto Y. 14-3-3 Interacts directly with and negatively regulates pro-apoptotic Bax. J Biol Chem. 2003,278(3):2058-65.
19. Tsuruta F, Sunayama J, Mori Y, Hattori S, Shimizu S, Tsujimoto Y, Yoshioka K, Masuyama N, Gotoh Y. JNK promotes Bax translocation to mitochondria through phosphorylation of 14-3-3 proteins. EMBO J. 2004, 23(8): 1889-99.
20. Gardino, A.K. et al. Structural determinants of 14-3-3 binding specificities and regulation of subcellular localization of 14-3-3-ligand complexes: a comparison of the X-ray crystal structures of all human 14-3-3 isoforms. Semin Cancer Biol. 2006, 16,173-182.
21. Siman R, Roberts VL, McNeil E. Biomarker evidence for mild central nervous system injury after surgically-induced circulation arrest. Brain Res. 2008,1213:1-11.
22. Siman R, Mclntosh TK, Soltesz KM. Proteins released from degenerating neurons are surrogate markers for acute brain damage. Neurobiol Dis. 2004, 16(2):311-20.
23. Yu F, Narasimhan P, Chan PH. Increased expression of a proline-rich Akt substrate (PRAS40) in human copper/zinc-superoxide dismutase transgenic rats protects motor neurons from death after spinal cord injury. J Cereb Blood Flow Metab. 2008,28(1):44-52.
24. Kamada H, Nito C, Endo H, Chan PH. Bad as a converging signaling molecule between survival PI3-K/Akt and death JNK in neurons after transient focal cerebral ischemia in rats. J Cereb Blood Flow Metab. 2007, 27(3):521-33
25. Saito A, Hayashi T, Okuno S, Nishi T, Chan PH. Modulation of proline-rich akt substrate survival signaling pathways by oxidative stress in mouse brains after transient focal cerebral ischemia. Stroke. 2006, 37(2):513-7.
26. Satoh J, Tabunoki H, Nanri Y, Arima K, Yamamura T.Human astrocytes express 14-3-3 sigma in response to oxidative and DNA-damaging stresses. Neurosci Res. 2006,56(1):61-72.
27. Wang XT, Pei DS, Xu J, Guan QH, Sun YF, Liu XM, Zhang GY. Opposing effects of Bad phosphorylation at two distinct sites by Akt1 and JNK 1/2 on ischemic brain injury.Cell Signal. 2007, 19(9): 1844-56.
28. Koh PO. Melatonin prevents the injury-induced decline of Akt/forkhead transcription factors phosphorylation. J Pineal Res. 2008,45(2): 199-203.
29. Koh PO. Melatonin attenuates the focal cerebral ischemic injury by inhibiting the dissociation of pBad from 14-3-3. J Pineal Res. 2008,44(1): 101-6.
30. Chen XQ, Fung YW, Yu AC. Association of 14-3-3gamma and phosphorylated bad attenuates injury in ischemic astrocytes. J Cereb Blood Flow Metab. 2005,25(3):338-47.
31. Chen XQ, Chen JG, Zhang Y, Hsiao WW, Yu AC. 14-3-3gamma is upregulated by in vitro ischemia and binds to protein kinase Raf in primary cultures of astrocytes. Glia.2003,42(4):315-24.
32. Chen XQ, Liu S, Qin LY, Wang CR, Fung YW, Yu AC. Selective regulation of 14-3-3 eta in primary culture of cerebral cortical neurons and astrocytes during development. J Neurosci Res. 2005, 79(1-2): 114-8.
33. Chen XQ, Yu AC. The association of 14-3-3gamma and actin plays a role in cell division and apoptosis in astrocytes. Biochem Biophys Res Commun. 2002,296(3):657-63.
34. Kawamoto Y, Akiguchi I, Tomimoto H, Shirakashi Y, Honjo Y, Budka H. Upregulated expression of 14-3-3 proteins in astrocytes from human cerebrovascular ischemic lesions. Stroke. 2006, 37(3):830-5.
35. Li H, Guo Y, Teng J, Ding M, Yu AC, Chen J. 14-3-3gamma affects dynamics and integrity of glial filaments by binding to phosphorylated GFAP. J Cell Sci. 2006, 119(Pt 21):4452-61.
36. Ye SQ, Lai XJ, Luo ZZ, Li L, Chen XQ (corresponding author). 14-3-3 protects ischemic neurons from apoptosis by transcriptional down-regulating Bax through beta-catenin. 2009, submitted.
37. Wu JS, Cheung WM, Lin TN.Ligand-activated peroxisome proliferator activated receptor-gamma protects against ischemic cerebral infarction and neuronal apoptosis by 14-3-3 epsilon upregulation. Circulation. 2009,119(8): 1124-34.
38. Downey JM, Cohen MV. Signal transduction in ischemic preconditioning. Adv Exp Med Biol. 1997,430:39.
39. Downey JM, Liu GS, Thornton JD. Adenosine and the anti-infarct effects of preconditioning. Cardiovasc Res, 1993, 27:3.
40. Mabanta L, Valane P, Borne J, et al. Initiation of remote microvascular preconditioning requires K(ATP) channel activity. Am J Physiol Heart Circ Physiol 2006, 290:H264.
41. Jiang Z, Zhang Y, Chen XQ, Lam PY, Yang H, Xu Q, Yu AC. Activation of Erk1/2 and Akt in astrocytes under ischemia. Biochem Biophys Res Commun. 2002,294(3):726-33.
42. QG Zhang, et al. Ischemic preconditioning negatively regulates plenty of SH3s-mixed lineage kinase 3-Racl complex and c-Jun N-terminal kinase 3 signaling via activation of Akt. Neuroscience, 2006, 143: 431-444.
43. CW Yang, et al. Ischemic preconditioning suppresses apoptosis of rabbit spinal neurocytes by inhibiting ASK1-14-3-3 dissociation. Neuroscience Letters, 2008, 441:267-271.
44. Shiga Y, Wakabayashi H, Miyazawa K, Kido H, Itoyama Y. 14-3-3 protein levels and isoform patterns in the cerebrospinal fluid of Creutzfeldt-Jakob disease patients in the progressive and terminal stages. J Clin Neurosci. 2006, 13(6):661-5.
45. Umahara T, Uchihara T, Tsuchiya K, Nakamura A, Iwamoto T, Ikeda K, Takasaki M. 14-3-3 proteins and zeta isoform containing neurofibrillary tangles in patients with Alzheimer's disease. Acta Neuropathol. 2004 , 108(4):279-86.
46. Santpere G, Puig B, Ferrer I. Oxidative damage of 14-3-3 zeta and gamma isoforms in Alzheimer's disease and cerebral amyloid angiopathy. Neuroscience. 2007,146(4): 1640-51.
47. Sato S, Chiba T, Sakata E, Kato K, Mizuno Y, Hattori N, Tanaka K. 14-3-3eta is a novel regulator of parkin ubiquitin ligase. EMBO J. 2006, 25(1):211-21.
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