PUMA-mediated mitochondrial apoptotic disruption by hypoxic postconditioning

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• 作者：YuZhen Li ; Qi Guo ; XiuHua Liu ; Chen Wang ; DanDan Song
• 关键词：Postconditioning ; PUMA ; Apoptosis ; Mitochondrial pathway ; Cardiomyocyte
• 刊名：Apoptosis
• 出版年：2015
• 出版时间：August 2015
• 年：2015
• 卷：20
• 期：8
• 页码：1026-1032
• 全文大小：1,156 KB
• 参考文献：1.Zhao ZQ, Corvera JS, Halkos ME, Kerendi F, Wang NP, Guyton RA et al (2003) Inhibition of myocardial injury by ischemic postconditioning during reperfusion: comparison with ischemic preconditioning. Am J Physiol Heart Circ Physiol 285:579-88View Article
  2.Kin H, Zhao ZQ, Sun HY, Wang NP, Corvera JS, Halkos ME et al (2004) Postconditioning attenuates myocardial ischemia-reperfusion injury by inhibiting events in the early minutes of reperfusion. Cardiovasc Res 62:74-5PubMed View Article
  3.Sun HY, Wang NP, Kerendi F, Halkos M, Kin H, Guyton RA et al (2005) Hypoxic postconditioning reduces cardiomyocyte loss by inhibiting ROS generation and intracellular Ca2+ overload. Am J Physiol Heart Circ Physiol 288:1900-908View Article
  4.Sun HY, Wang NP, Halkos M, Kerendi F, Kin H, Guyton RA et al (2006) Postconditioning attenuates cardiomyocyte apoptosis via inhibition of JNK and p38 mitogen-activated protein kinase signaling pathways. Apoptosis 11:1583-593PubMed View Article
  5.Gustafsson AB, Gottlieb RA (2008) Heart mitochondria: gates of life and death. Cardiovasc Res 77:334-43PubMed View Article
  6.Crow MT, Kartik M, Nam YJ, Kitsis RN (2004) The mitochondrial death pathway and cardiac myocyte apoptosis. Circ Res 95:957-70PubMed View Article
  7.Gomez L, Paillard M, Thibault H, Derumeaux G, Ovize M (2008) Inhibition of GSK3beta by postconditioning is required to prevent opening of the mitochondrial permeability transition pore during reperfusion. Circulation 117(21):2761-768PubMed View Article
  8.Juhaszova M, Zorov DB, Yaniv Y, Nuss HB, Wang S, Sollott SJ (2009) Role of glycogen synthase kinase-3beta in cardioprotection. Circ Res 104(11):1240-252PubMed Central PubMed View Article
  9.Perrelli MG, Pagliaro P, Penna C (2011) Ischemia/reperfusion injury and cardioprotective mechanisms: role of mitochondria and reactive oxygen species. World J cardiol 3(6):186-00PubMed Central PubMed View Article
  10.Yu J, Zhang L (2009) PUMA, a potent killer with or without p53. Oncogene 27:S71–S83View Article
  11.Mandl A, Huong Pham L, Toth K, Zambetti G, Erhardt P (2011) Puma deletion delays cardiac dysfunction in murine heart failure models through attenuation of apoptosis. Circulation 124(1):31-9PubMed View Article
  12.Toth A, Jeffers JR, Nickson P, Min JY, Morgan JP, Zambetti GP et al (2006) Targeted deletion of PUMA attenuates cardiomyocyte death and improves cardiac function during ischemia-reperfusion. Am J Physiol Heart Circ Physiol 291:H52–H60PubMed View Article
  13.Li Y, Liu X, Rong F (2011) PUMA mediates the apoptotic signal of hypoxia/reoxygenation in cardiomyocytes through mitochondrial pathway. Shock 35(6):579-84PubMed View Article
  14.Liu XH, Zhang ZY, Sun S, Wu XD (2008) Ischemic postconditioning protects myocardium from ischemia/reperfusion injury through attenuating endoplasmic reticulum stress. Shock 30(4):422-27PubMed View Article
  15.Li Y, Lu D, Tan W, Wang JX, Li P (2008) p53 initiates apoptosis by transcriptionally targeting the antiapoptotic protein ARC. Mol Cell Biol 28(2):564-74PubMed Central PubMed View Article
  16.Salvioli S, Ardizzoni A, Franceschi C, Cossarizza A (1997) JC-1, but not DiOC6(3) or rhodamine 123, is a reliable fluorescent probe to assess delta psi changes in intact cells: implications for studies on mitochondrial functionality during apoptosis. FEBS Lett 411:77-2PubMed View Article
  17.Li Y, Lv Z, Liu X, Wang C, Li N, Song D et al (2013) Hypoxic postconditioning inhibits endoplasmic reticulum stress-mediated cardiomyocyte apoptosis by targeting PUMA. Shock 39(3):299-03PubMed View Article
  18.Aon MA, Cortassa S, Akar FG, O’Rourke B (2006) Mitochondrial criticality: a new concept at the turning point of life or death. Biochim Biophys Acta 1762(2):232-40PubMed Central PubMed View Article
  19.Murphy E, Steenbergen C (2011) What makes the mitochondria a killer? Can we condition them to be less destructive? Biochim Biophys Acta 1813(7):1302-308PubMed Central PubMed View Article
  20.Li Y, Ge X, Liu X (2009) The cardioprotective effect of postconditioning is mediated by ARC through inhibiting mitochondrial apoptotic pathway. Apoptosis 14(2):164-72PubMed View Article
  21.Jin HJ, Xie XL, Ye JM, Li CG (2013) Tanshinone IIA and cryptotanshinone protect against hypoxia-induced mitochondrial apoptosis in H9c2 cells. PLoS One 8(1):e51720PubMed Central PubMed View Article
  22.Garrison SP, Phillips DC, Jeffers JR, Chipuk JE, Parsons MJ, Rehg JE et al (2012) Genetically defining the mechanism of Puma- and Bim-induced apoptosis. Cell Death Differ 19(4):642-49PubMed Central PubMed View Article
  23.Nakano K, Vousden KH (2001) PUMA, a novel proapoptotic gene, is induced by p53. Mol Cell 7:683-94PubMed View Article
  
• 作者单位：YuZhen Li (1)
  Qi Guo (1)
  XiuHua Liu (1)
  Chen Wang (1)
  DanDan Song (1)
  
  1. Department of Pathophysiology, Institute of Basic Medical Science, PLA General Hospital, Beijing, 100853, China
  
• 刊物类别：Medicine
• 刊物主题：Medicine & Public Health
  Oncology
  Cancer Research
  Cell Biology
  Biochemistry
  Virology
  
• 出版者：Springer Netherlands
• ISSN：1573-675X

文摘

Postconditioning can reduce ischemia–reperfusion (I/R)-induced cardiomyocyte apoptosis by targeting mitochondria. p53 upregulated modulator of apoptosis (PUMA) is involved in lethal I/R injury. Here, we hypothesized that postconditioning might inhibit mitochondrial pathway-mediated cardiomyocyte apoptosis by controlling PUMA expression. The cultured neonatal rat cardiomyocytes underwent 3?h of hypoxia and 3?h of reoxygenation. Postconditioning consisted of three cycles of 5?min reoxygenation and 5?min hypoxia after prolonged hypoxia. Hypoxic postconditioning reduced the levels of PUMA mRNA and protein. Concomitantly, the loss of mitochondrial membrane potential, cytochrome c release and caspase-3 activation were decreased significantly by postconditioning. Overexpression of PUMA increased greatly not only the number of apoptotic cardiomyocytes, but also the collapse of mitochondrial membrane potential, cytochrome c release and caspase-3 activation under postconditioning condition. The data suggest that reduction of PUMA expression mediates the endogenous cardioprotective mechanisms of postconditioning by disrupting mitochondrial apoptotic pathway.