MicroRNA-15a/b are up-regulated in response to myocardial ischemia/reperfusion injury.
MicroRNA-15a/b are up-regulated in response to myocardial ischemia/reperfusion injury.
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DOI：
10.3724/sp.j.1263.2012.00028
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发表时间：
2012-03
期刊：
影响因子：
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通讯作者：
Wang Y
中科院分区：
文献类型：
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作者：
Liu LF;Liang Z;Lv ZR;Liu XH;Bai J;Chen J;Chen C;Wang Y
多项研究表明，miR-15 a、miR-15 b和miR-16可能是细胞凋亡的重要调控因子。由于减少细胞凋亡可以保护心肌，缩小梗死面积，本研究旨在探讨这些miRNAs是否参与了心肌缺血再灌注（I/R）损伤的调控。在体采用TUNEL法检测缺血/再灌注小鼠心肌细胞凋亡，在体外采用Annexin V/PI双染流式细胞术检测缺氧/复氧（H/R）培养心肌细胞凋亡。采用Taqman实时定量PCR方法检测miR-15 a/15 b/16是否参与心肌I/R和H/R的调节。与对照组相比，I/R或H/R诱导的心肌细胞凋亡在体内（24.4% ± 9.4% vs.2.2% ± 1.9%，P < 0.01，n = 5）和体外（14.12% ± 0.92% vs.2.22% ± 0.08%）均显著增加。在小鼠I/R模型中，miR-15 a和miR-15 b的表达增加，但miR-16的表达没有增加，并且在H/R模型中结果一致。我们的数据表明miR-15和miR-15 B在心脏I/R损伤中表达上调，因此，下调miR-15 a/B可能是减少心脏I/R损伤诱导的心肌细胞凋亡的一种有前景的策略。
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. 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. Compared to those of the controls, I/R or H/R induced apoptosis of cardiomyocytes was significantly increased 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. 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.