线粒体能量代谢相关miRNA的研究进展
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摘要
线粒体为真核细胞的能量工厂,其能量代谢与细胞凋亡、自噬和衰老等过程密切相关,在疾病的发生发展以及后续治疗中也发挥着重要作用。microRNAs(miRNAs)为一类广泛存在于真核生物中的单链RNA,可通过降解靶基因或抑制靶基因的翻译来调节蛋白表达。近年来多项研究表明,miRNA还可通过调节线粒体相关基因的表达,调控线粒体的结构及功能,影响线粒体的能量代谢。本文就miRNA的作用机制及其与线粒体能量代谢关系的研究进展作一综述。
Mitochondria are the energy factories for eukaryotic cells. Mitochondrial energy metabolism is closely related to the apoptosis,autophagy and aging of cells,which plays an important role in the development of disease and subsequent treatment. MiRNAs are single-stranded RNAs which exist widely in eukaryotes and modulate the expression of protein by degrading target genes or inhibiting translation. In recent years,several studies have shown that miRNA can also regulate the structure and function of mitochondria and affect the energy metabolism of mitochondria by regulating the expression of mitochondrial related genes. This paper reviews the progress in research on mechanism of miRNA and its relationship to mitochondrial energy metabolism
Mitochondria are the energy factories for eukaryotic cells. Mitochondrial energy metabolism is closely related to the apoptosis,autophagy and aging of cells,which plays an important role in the development of disease and subsequent treatment. MiRNAs are single-stranded RNAs which exist widely in eukaryotes and modulate the expression of protein by degrading target genes or inhibiting translation. In recent years,several studies have shown that miRNA can also regulate the structure and function of mitochondria and affect the energy metabolism of mitochondria by regulating the expression of mitochondrial related genes. This paper reviews the progress in research on mechanism of miRNA and its relationship to mitochondrial energy metabolism
引文
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[3] KAUPPILA T E S, KAUPPILA J H K, LARSSON N G. Mammalian mitochondria and aging:an update[J]. Cell Metab,2017, 25(1):57-71.
[4] XIE Q, SU J, JIAO B, et al. ABT737 reverses cisplatin resistance by regulating ER-mitochondria Ca2+signal transduction in human ovarian cancer cells[J]. Int J Oncol,2016,49(6):2507-2519.
[5] GOMEZ-SUAGA P, PAILLUSSON S, STOIC A R, et al. The ER-mitochondria tethering complex VAPB-PTPIP51 regulates autophagy[J]. Curr Biol, 2017, 27(3):371-385.
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[7] DOMINIC E A, RAMEZANI A, ANKER S D, et al. Mitochondrial cytopathies and cardiovascular disease[J]. Heart,2014,100(8):611-618.
[8] NYAYANIT D, GADGIL C J. Mathematical modeling of combinatorial regulation suggests that apparent positive regulation of targets by miRNA could be an artifact resulting from competition for mRNA[J]. RNA, 2015, 21(3):307-319.
[9] CHEN G, UMELO I A, LV S, et al. miR-146a inhibits cell growth, cell migration and induces apoptosis in non-small cell lung cancer cells[J]. PLoS One, 2013, 8(3):e60317. doi:10.1371/journal.pone.0060317.
[10] ZHANG N, WEI X, XU L. miR-150 promotes the proliferation of lung cancer cells by targeting P53[J]. FEBS Lett, 2013,587(15):2346-2351.
[11] ARANHA M M,SANTOS D M,SOLA S, et al. miR-34a regulates mouse neural stem cell differentiation[J]. PLoS One,2011, 6(8):e21396. doi:10.1371/journal.pone.0021396.
[12] ZHOU Q, CHEN F, ZHAO J, et al.Long non-coding RNA PVT1promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195[J]. Oncotarget,2016,7(50):82620-82633.
[13] SIENGDEE P, TRAKOOLJUL N, MURANI E, et al. MicroRNAs regulate cellular ATP levels by targeting mitochondrial energy metabolism genes during C2C12 myoblast differentiation[J]. PLoS One, 2015, 10(5):e0127850. doi:10.1371/journal.pone.0127850.
[14] DAHLMANS D, HOUZELLE A, ANDREUX P, et al. An unbiased silencing screen in muscle cells identifies miR-320a,miR-150,miR-196b,and miR-34c as regulators of skeletal muscle mitochondrial metabolism[J]. Mol Metab, 2017, 6(11):1429-1442.
[15] WANG H, ZHANG L, GUO X, et al. MiR-195 modulates oxidative stress-induced apoptosis and mitochondrial energy production in human trophoblasts via flavin adenine dinucleotidedependent oxidoreductase domain-containing protein 1 and pyruvate dehydrogenase phosphatase regulatory subunit[J]. J Hypertens,2018,36(2):306-318.
[16] LEE Y S, NAKAHARA K, PHAM J W, et al. Distinct roles for Drosophila Dicer-1 and Dicer-2 in the siRNA/miRNA silencing pathways[J]. Cell,2004,117(1):69-81.
[17] LEE Y, KIM M, HAN J, et al. MicroRNA genes are transcribed by RNA polymeraseⅡ[J]. EMBO J, 2004, 23(20):4051-4060.
[18] GRUND S E, POLYCARPOU-SCHWARZ M, LUO C, et al.Rare Drosha splice variants are deficient in microRNA processing but do not affect general microRNA expression in cancer cells[J]. Neoplasia, 2012, 14(3):238-248.
[19] LEE Y, JEON K, LEE J T, et al. MicroRNA maturation:stepwise processing and subcellular localization[J]. EMBO J,2002, 21(17):4663-4670.
[20] YEOM K H, LEE Y, HAN J, et al. Characterization of DGCR8/Pasha, the essential cofactor for Drosha in primary miRNA processing[J]. Nucleic Acids Res, 2006, 34(16):4622-4629.
[21] HAUSSER J, ZAVOLAN M. Identification and consequences of miRNA-target interactions-Beyond repression of gene expression[J]. Nat Rev Genet, 2014, 15(9):599-612.
[22] LEUNG A K, SHARP P A. microRNAs:a safeguard against turmoil[J]. Cell, 2007, 130(4):581-585.
[23] AKBARI MOQADAM F, PIETERS R, DEN BOER M L. The hunting of targets:challenge in miRNA research[J]. Leukemia, 2013, 27(1):16-23.
[24] TOSCANO-GARIBAY J D, AQUINO-JARQUIN G. Transcriptional regulation mechanism mediated by miRNA-DNAoDNA triplex structure stabilized by Argonaute[J]. Biochim Biophys Acta, 2014, 1839(11):1079-1083.
[25] QIU G Z, JIN M Z, DAI J X, et al. Reprogramming of the tumor in the hypoxic niche:The emerging concept and associated therapeutic strategies[J]. Trends Pharmacol Sci,2017,38(8):669-686.
[26] CHAN S Y, ZHANG Y Y, HEMANN C, et al. MicroRNA-210controls mitochondrial metabolism during hypoxia by repressing the iron-sulfur cluster assembly proteins ISCU1/2[J]. Cell Metab, 2009, 10(4):273-284.
[27] COLLEONI F, PADMANABHAN N, YUNG H W, et al. Suppression of mitochondrial electron transport chain function in the hypoxic human placenta:a role for miRNA-210 and protein synthesis inhibition[J]. PLoS One,2013,8(1):e55194. doi:10.1371/journal.pone.0055194.
[28] QIAO A, KHECHADURI A, MUTHARASAN R K, et al. MicroRNA-210 decreases heme levels by targeting ferrochelatase in cardiomyocytes[J]. J Am Heart Assoc,2013,2(2):e00-0121. doi:10.1161/JAHA.113.000121.
[29] ULLMANN P, QURESHI-BAIG K, RODRIGUEZ F, et al. Hypoxia-responsive miR-210 promotes self-renewal capacity of colon tumor-initiating cells by repressing ISCU and by inducing lactate production[J]. Oncotarget,2016,7(40):65454-65470.
[30] LILL R, SRINIVASAN V, MUHLENHOFF U. The role of mitochondria in cytosolic-nuclear iron-sulfur protein biogenesis and in cellular iron regulation[J]. Curr Opin Microbiol, 2014,22(12):111-119.
[31] GUO W J, LIAN S, GUO J R, et al. Biological function prediction of mir-210 in the liver of acute cold stress rat[J].Acta Physiol Sin,2016,68(2):165-170.(in Chinese)郭文晋,连帅,郭景茹,等.急性冷应激大鼠肝脏中mir-210学物的生学功能预测[J].生理学报,2016, 68(2):165-170.
[32] PUISSEGUR M P, MAZURE N M, BERTERO T, et al. miR-210 is overexpressed in late stages of lung cancer and mediates mitohondrial alterations associated with modulation of HIF-1activity[J]. Cell Death&Differentiation, 2011, 18(3):465.
[33] QIN W. miR-17-5p alleviates mitochondrial dysfunction resulted from chronic intermittent hypoxia in genioglossus muscle satellite cells of rats[D]. Xi'an:The Fourth Military Medical University, 2015.(in Chinese)秦文.miR-17-5p在低氧环境下影响颏舌肌肌卫星细胞线粒体功能的初步研究[D].陕西西安:第四军医大学,2015.
[34] DANIELE T, HURBAIN I, VAGO R, et al. Mitochondria and melanosomes establish physical contacts modulated by Mfn2and involved in organelle biogenesis[J]. Curr Biol Cb, 2014,24(4):393-403.
[35] WANG X D. Dopamine-induced apoptosis in human melanocytes involves dysfunction of mitofilin:a possible cause for melanocytes loss in vitiligo[D]. Xi'an:The Fourth Military Medical University, 2010.(in Chinese)王旭东.线粒体内膜蛋白Mitofilin在白癜风发病中作用研究[D].陕西西安:第四军医大学,2010.
[36] SAHOO A, LEE B, BONIFACE K, et al. MicroRNA-211 regulates oxidative phosphorylation and energy metabolism in human vitiligo[J]. J Investig Dermatol, 2017, 137(9):1965-1974.
[37] MAZAR J, QI F, LEE B, et al. MicroRNA 211 functions as a metabolic switch in human melanoma cells[J]. Mol Cell Biol,2016, 36(7):1090-1108.
[38] AOI W, NAITO Y, MIZUSHIMA K, et al. The microRNA miR-696 regulates PGC-1{alpha}in mouse skeletal muscle in response to physical activity[J]. Am J Physiol Endocrinol Metab,2010, 298(4):E799-E806. doi:10.1152/ajpendo.00448.2009.
[39] YAMAMOTO H, MORINO K, NISHIO Y, et al. MicroRNA-494 regulates mitochondrial biogenesis in skeletal muscle through mitochondrial transcription factor A and Forkhead box j3[J]. Am J Physiol Endocrinol Metab,2012,303(12):E1419-E1427.
[40] YOHWINKEL C U, LECUONA E, SUN H, et al. Elevated C02 levels cause mitochondrial dysfunction and impair cell proliferation[J]. J Biol Chem, 2011, 286(43):37067-37076.
[41] GOUD M R, ZHANG A H. Role of microRNA in the regulation of mitochondrial functions[J]. J Sci Lett,2015,3(2):83-88.
[2] HOCKENBERY D M, GIEDT C D, O'NEILL J W, et al. Mitochondria and apoptosis:new therapeutic targets[J]. Adv Cancer Res, 2002, 85:203-242.
[3] KAUPPILA T E S, KAUPPILA J H K, LARSSON N G. Mammalian mitochondria and aging:an update[J]. Cell Metab,2017, 25(1):57-71.
[4] XIE Q, SU J, JIAO B, et al. ABT737 reverses cisplatin resistance by regulating ER-mitochondria Ca2+signal transduction in human ovarian cancer cells[J]. Int J Oncol,2016,49(6):2507-2519.
[5] GOMEZ-SUAGA P, PAILLUSSON S, STOIC A R, et al. The ER-mitochondria tethering complex VAPB-PTPIP51 regulates autophagy[J]. Curr Biol, 2017, 27(3):371-385.
[6] JOHANNSEN D L, RAVUSSIN E. The role of mitochondria in health and disease[J]. Curr Opin Pharmacol, 2009, 9(6):780-786.
[7] DOMINIC E A, RAMEZANI A, ANKER S D, et al. Mitochondrial cytopathies and cardiovascular disease[J]. Heart,2014,100(8):611-618.
[8] NYAYANIT D, GADGIL C J. Mathematical modeling of combinatorial regulation suggests that apparent positive regulation of targets by miRNA could be an artifact resulting from competition for mRNA[J]. RNA, 2015, 21(3):307-319.
[9] CHEN G, UMELO I A, LV S, et al. miR-146a inhibits cell growth, cell migration and induces apoptosis in non-small cell lung cancer cells[J]. PLoS One, 2013, 8(3):e60317. doi:10.1371/journal.pone.0060317.
[10] ZHANG N, WEI X, XU L. miR-150 promotes the proliferation of lung cancer cells by targeting P53[J]. FEBS Lett, 2013,587(15):2346-2351.
[11] ARANHA M M,SANTOS D M,SOLA S, et al. miR-34a regulates mouse neural stem cell differentiation[J]. PLoS One,2011, 6(8):e21396. doi:10.1371/journal.pone.0021396.
[12] ZHOU Q, CHEN F, ZHAO J, et al.Long non-coding RNA PVT1promotes osteosarcoma development by acting as a molecular sponge to regulate miR-195[J]. Oncotarget,2016,7(50):82620-82633.
[13] SIENGDEE P, TRAKOOLJUL N, MURANI E, et al. MicroRNAs regulate cellular ATP levels by targeting mitochondrial energy metabolism genes during C2C12 myoblast differentiation[J]. PLoS One, 2015, 10(5):e0127850. doi:10.1371/journal.pone.0127850.
[14] DAHLMANS D, HOUZELLE A, ANDREUX P, et al. An unbiased silencing screen in muscle cells identifies miR-320a,miR-150,miR-196b,and miR-34c as regulators of skeletal muscle mitochondrial metabolism[J]. Mol Metab, 2017, 6(11):1429-1442.
[15] WANG H, ZHANG L, GUO X, et al. MiR-195 modulates oxidative stress-induced apoptosis and mitochondrial energy production in human trophoblasts via flavin adenine dinucleotidedependent oxidoreductase domain-containing protein 1 and pyruvate dehydrogenase phosphatase regulatory subunit[J]. J Hypertens,2018,36(2):306-318.
[16] LEE Y S, NAKAHARA K, PHAM J W, et al. Distinct roles for Drosophila Dicer-1 and Dicer-2 in the siRNA/miRNA silencing pathways[J]. Cell,2004,117(1):69-81.
[17] LEE Y, KIM M, HAN J, et al. MicroRNA genes are transcribed by RNA polymeraseⅡ[J]. EMBO J, 2004, 23(20):4051-4060.
[18] GRUND S E, POLYCARPOU-SCHWARZ M, LUO C, et al.Rare Drosha splice variants are deficient in microRNA processing but do not affect general microRNA expression in cancer cells[J]. Neoplasia, 2012, 14(3):238-248.
[19] LEE Y, JEON K, LEE J T, et al. MicroRNA maturation:stepwise processing and subcellular localization[J]. EMBO J,2002, 21(17):4663-4670.
[20] YEOM K H, LEE Y, HAN J, et al. Characterization of DGCR8/Pasha, the essential cofactor for Drosha in primary miRNA processing[J]. Nucleic Acids Res, 2006, 34(16):4622-4629.
[21] HAUSSER J, ZAVOLAN M. Identification and consequences of miRNA-target interactions-Beyond repression of gene expression[J]. Nat Rev Genet, 2014, 15(9):599-612.
[22] LEUNG A K, SHARP P A. microRNAs:a safeguard against turmoil[J]. Cell, 2007, 130(4):581-585.
[23] AKBARI MOQADAM F, PIETERS R, DEN BOER M L. The hunting of targets:challenge in miRNA research[J]. Leukemia, 2013, 27(1):16-23.
[24] TOSCANO-GARIBAY J D, AQUINO-JARQUIN G. Transcriptional regulation mechanism mediated by miRNA-DNAoDNA triplex structure stabilized by Argonaute[J]. Biochim Biophys Acta, 2014, 1839(11):1079-1083.
[25] QIU G Z, JIN M Z, DAI J X, et al. Reprogramming of the tumor in the hypoxic niche:The emerging concept and associated therapeutic strategies[J]. Trends Pharmacol Sci,2017,38(8):669-686.
[26] CHAN S Y, ZHANG Y Y, HEMANN C, et al. MicroRNA-210controls mitochondrial metabolism during hypoxia by repressing the iron-sulfur cluster assembly proteins ISCU1/2[J]. Cell Metab, 2009, 10(4):273-284.
[27] COLLEONI F, PADMANABHAN N, YUNG H W, et al. Suppression of mitochondrial electron transport chain function in the hypoxic human placenta:a role for miRNA-210 and protein synthesis inhibition[J]. PLoS One,2013,8(1):e55194. doi:10.1371/journal.pone.0055194.
[28] QIAO A, KHECHADURI A, MUTHARASAN R K, et al. MicroRNA-210 decreases heme levels by targeting ferrochelatase in cardiomyocytes[J]. J Am Heart Assoc,2013,2(2):e00-0121. doi:10.1161/JAHA.113.000121.
[29] ULLMANN P, QURESHI-BAIG K, RODRIGUEZ F, et al. Hypoxia-responsive miR-210 promotes self-renewal capacity of colon tumor-initiating cells by repressing ISCU and by inducing lactate production[J]. Oncotarget,2016,7(40):65454-65470.
[30] LILL R, SRINIVASAN V, MUHLENHOFF U. The role of mitochondria in cytosolic-nuclear iron-sulfur protein biogenesis and in cellular iron regulation[J]. Curr Opin Microbiol, 2014,22(12):111-119.
[31] GUO W J, LIAN S, GUO J R, et al. Biological function prediction of mir-210 in the liver of acute cold stress rat[J].Acta Physiol Sin,2016,68(2):165-170.(in Chinese)郭文晋,连帅,郭景茹,等.急性冷应激大鼠肝脏中mir-210学物的生学功能预测[J].生理学报,2016, 68(2):165-170.
[32] PUISSEGUR M P, MAZURE N M, BERTERO T, et al. miR-210 is overexpressed in late stages of lung cancer and mediates mitohondrial alterations associated with modulation of HIF-1activity[J]. Cell Death&Differentiation, 2011, 18(3):465.
[33] QIN W. miR-17-5p alleviates mitochondrial dysfunction resulted from chronic intermittent hypoxia in genioglossus muscle satellite cells of rats[D]. Xi'an:The Fourth Military Medical University, 2015.(in Chinese)秦文.miR-17-5p在低氧环境下影响颏舌肌肌卫星细胞线粒体功能的初步研究[D].陕西西安:第四军医大学,2015.
[34] DANIELE T, HURBAIN I, VAGO R, et al. Mitochondria and melanosomes establish physical contacts modulated by Mfn2and involved in organelle biogenesis[J]. Curr Biol Cb, 2014,24(4):393-403.
[35] WANG X D. Dopamine-induced apoptosis in human melanocytes involves dysfunction of mitofilin:a possible cause for melanocytes loss in vitiligo[D]. Xi'an:The Fourth Military Medical University, 2010.(in Chinese)王旭东.线粒体内膜蛋白Mitofilin在白癜风发病中作用研究[D].陕西西安:第四军医大学,2010.
[36] SAHOO A, LEE B, BONIFACE K, et al. MicroRNA-211 regulates oxidative phosphorylation and energy metabolism in human vitiligo[J]. J Investig Dermatol, 2017, 137(9):1965-1974.
[37] MAZAR J, QI F, LEE B, et al. MicroRNA 211 functions as a metabolic switch in human melanoma cells[J]. Mol Cell Biol,2016, 36(7):1090-1108.
[38] AOI W, NAITO Y, MIZUSHIMA K, et al. The microRNA miR-696 regulates PGC-1{alpha}in mouse skeletal muscle in response to physical activity[J]. Am J Physiol Endocrinol Metab,2010, 298(4):E799-E806. doi:10.1152/ajpendo.00448.2009.
[39] YAMAMOTO H, MORINO K, NISHIO Y, et al. MicroRNA-494 regulates mitochondrial biogenesis in skeletal muscle through mitochondrial transcription factor A and Forkhead box j3[J]. Am J Physiol Endocrinol Metab,2012,303(12):E1419-E1427.
[40] YOHWINKEL C U, LECUONA E, SUN H, et al. Elevated C02 levels cause mitochondrial dysfunction and impair cell proliferation[J]. J Biol Chem, 2011, 286(43):37067-37076.
[41] GOUD M R, ZHANG A H. Role of microRNA in the regulation of mitochondrial functions[J]. J Sci Lett,2015,3(2):83-88.
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