MiR-204 regulates cardiomyocyte autophagy induced by ischemia-reperfusion through LC3-II.

MiR-204 regulates cardiomyocyte autophagy induced by ischemia-reperfusion through LC3-II.
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MiR-204通过LC3-II调节缺血再灌注诱导的心肌细胞自噬

DOI:
10.1186/1423-0127-18-35
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发表时间:
2011-06-01
影响因子:
11
通讯作者:
Ni X
Ni X
中科院分区:
医学1区
文献类型:
--
作者:
Xiao J;Zhu X;He B;Zhang Y;Kang B;Wang Z;Ni X

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自噬在心肌缺血再灌注损伤中起重要作用。因此,除了抗凋亡外,抑制自噬对心肌细胞的保护也具有重要意义。已有研究表明,miRNA在缺血再灌注过程中可保护心肌细胞免于凋亡,但其是否具有抗自噬作用尚不清楚。本研究的目的是探讨miR-204是否通过调节心肌IR损伤过程中自噬体的标志物LC 3-II蛋白来调节自噬。成年SD大鼠随机分为对照组和IR组。IR组结扎冠状动脉左前降支30 min,松开结扎线再灌注2 h。RT-PCR检测miR-204的表达,Western-blot检测LC 3蛋白的表达。我们发现IR诱导心肌细胞自噬,同时下调miR-204和上调LC 3-II蛋白。而且,我们已经发现LC 3-II蛋白受miR-204调节,使用miR-204模拟物或AMO-204转移到心肌细胞中的方法,之前。这些研究为miR-204在IR过程中通过LC 3-II蛋白调节自噬提供了重要证据。
Autophagy plays a significant role in myocardial ischemia-reperfusion (IR) injury. So it is important to inhibit autophagy to protect cardiomyocytes besides anti-apoptosis. MiRNA has been demonstrated to protect cardiomyocytes against apoptosis during IR, while whether it has anti-autophagy effect has not been known. The aim of this study was to investigate whether miR-204 regulated autophagy by regulating LC3-II protein, which is the marker of autophagosome during myocardial IR injury. Adult SD rats were randomized to Control and IR groups. IR group was treated with 30 min ischemia by ligating the left anterior descending coronary artery, followed by 2 h reperfusion by loosing the ligation. The expression of miR-204 was measured by RT-PCR, and LC3 protein was measured by western-blot. We found that IR induced cardiomyocytes autophagy, together with down-regulation of miR-204 and up-regulation of LC3-II protein. And, we have found that LC3-II protein was regulated by miR-204, using the method of transferring miR-204 mimic or AMO-204 into the cardiomyocytes, before. These studies provided evidence that miR-204 played an important role in regulating autophagy through LC3-IIprotein during IR.
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