期刊文献+

MicroRNA-15a/b are up-regulated in response to myocardial ischemia/reperfusion injury 被引量:15

MicroRNA-15a/b are up-regulated in response to myocardial ischemia/reperfusion injury
下载PDF
导出
摘要 ObjectiveSeveral 研究显示了 miR-15a, miR-15b 和 miR-16 可以是 apoptosis 的重要管理者。后来稀释 apoptosis 能保护心肌层和还原剂梗塞尺寸,现在的学习被瞄准发现是否这些 miRNAs 参予调整心肌的局部缺血灌注( I/R )在受到 I/R 的老鼠心的 injury.MethodsApoptosis 被 TUNEL 试金在 vivo 检测,当流动 cytometry 分析由 Annexin V/PI 列在后面时,在 vitro 的两倍污点被用来在受到 hypoxia/reoxygenation ( H/R )的有教养的 cardiomyocytes 检测 apoptosis 。Taqman 即时量的 PCR 被用来证实 miR-15a/15b/16 是否涉及心脏的 I/R 的规定,控制, I/R 或 H/R 的到那些的 H/R.ResultsCompared 导致了 cardiomyocytes 的 apoptosis 显著地在 vivo 两个都被增加(24.4%±9.4% 对 2.2%±1.9% , P <0.01, n = 5 ) 并且在 vitro (14.12%±0.92% 对 2.22%±0.08%) 。 miR-15a 和 miR-15b 的表达式,然而并非 miR-16 ,在鼠标 I/R 模型,和结果被增加在 H/R model.ConclusionsOur 数据是一致的显示因此, miR-15 和 miR-15b 响应心脏的 I/R 损害是起来调整的 miR-15a/b 的下面规定可以是有希望的策略减少心脏的 I/R 损害导致的心肌的 apoptosis 。 Objective Several studies have indicated that miR-15a,miR-15b and miR-16 may be the important regulators of apoptosis.Since attenuate apoptosis could protect myocardium and reduce infarction size,the present study was aimed to find out whether these miRNAs participate in regulating myocardial ischemia reperfusion (I/R) injury.Methods Apoptosis in mice hearts subjected to I/R was detected by TUNEL assay in vivo,while flow cytometry analysis followed by Annexin V/PI double stain in vitro was used to detect apoptosis in cultured cardiomyocytes which were subjected to hypoxia/reoxygenation (H/R).Taqman real-time quantitative PCR was used to confirm whether miR-15a/15b/16 were involved in the regulation of cardiac I/R and H/R.Results Compared to those of the controls,I/R or H/R induced apoptosis of cardiomyocytes was significantly iucreased both in vivo (24.4% ± 9.4% vs.2.2% ± 1.9%,P < 0.01,n =5) and in vitro (14.12% ±0.92% vs.2.22% ± 0.08%).The expression of miR-15a and miR-15b,but not miR-16,was increased in the mice I/R model,and the results were consistent in the H/R model.Conclusions Our data indicate miR-15 and miR-15b are up-regulated in response to cardiac I/R injury,therefore,down-regulation of miR- 15a/b may be a promising strategy to reduce myocardial apoptosis induced by cardiac I/R injury.
出处 《Journal of Geriatric Cardiology》 SCIE CAS CSCD 2012年第1期28-32,共5页 老年心脏病学杂志(英文版)
关键词 缺血 再灌注损伤 心肌梗死 心肌细胞凋亡 心肌缺血再灌注 流式细胞仪分析 ANNEXIN 实时定量PCR TUNEL法 miR-15a/b Apoptosis Myocardial reperfusion injury Ischemia/Reperfusion injury
  • 相关文献

参考文献23

  • 1Bartel DP. MicroRNAs: genomics, biogenesis, mechanism, and function. Cell 2004; 116: 281-297.
  • 2Yi R, Qin Y, Macara IG, et al. Exportin-5 mediates the nuclear export of pre-microRNAs and short hairpin RNAs. Genes Dev 2003; 17: 3011-3016.
  • 3Hutvagner G, Mclachlan J, Pasquinelli AE, et al. A cellular function for the RNA-interference enzyme Dicer in the maturation of the let-7 small temporal RNA. Science 2001; 293: 834-838.
  • 4Bartel DP. MicroRNAs: target recognition and regulatory functions. Cell 2009; 136:215-233.
  • 5Valencia-Sanchez MA, Liu J, Hannon GJ, et al. Control of translation and mRNA degradation by miRNAs and siRNAs. Genes Dev 2006; 20: 515-524.
  • 6Small E M, Frost RJ, Olson EN. MicroRNAs add a new dimension to cardiovascular disease. Circulation 2010; 121: 1022-1032.
  • 7Condorelli G, Latronico MV, Dorn GN. microRNAs in heart disease: putative novel therapeutic targets? Eur Heart J 2010; 31:649-658.
  • 8Latronico MV, Catalucci D, Condorelli G. Emerging role of microRNAs in cardiovascular biology. Circ Res 2007; 101: 1225-1236.
  • 9van Rooij E, Sutherland LB, Thatcher JE, et al. Dysregulation of microRNAs after myocardial infarction reveals a role of miR-29 in cardiac fibrosis. Proc Natl Acad Sci USA 2008; 105: 13027-13032.
  • 10Roy S, Khanna S, Hussain S R, et al. MicroRNA expression in response to murine myocardial infarction: miR-21 regulates fibroblast metalloprotease-2 via phosphatase and tensin homologue. Cardiovasc Res 2009; 82: 21-29.

同被引文献15

引证文献15

二级引证文献79

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部