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瓣膜置换手术期间远程缺血预处理诱导右心房中与凋亡相关的微小RNA变化。

Apoptosis-related microRNA changes in the right atrium induced by remote ischemic perconditioning during valve replacement surgery.

作者信息

Hu Qinghua, Luo Wanjun, Huang Lingjin, Huang Rimao, Chen Ri

机构信息

Department of cardiovascular surgery, Xiangya Hospital, Central-South University, Changsha, Hunan, China, 410078.

出版信息

Sci Rep. 2016 Jan 7;6:18959. doi: 10.1038/srep18959.

Abstract

We previously found that remote ischemic perconditioning (RIPerc) was effective in attenuating myocardial injury during cardiac surgery. Given that microRNAs (miRs) act as an important player in ischemic/reperfusion (I/R) injury and apoptosis, this study aimed to investigate whether RIPerc reduces apoptosis in atrial myocardium and which apoptosis-related miRs are involved during valve replacement surgery. Here, we demonstrated that RIPerc inhibited apoptosis in atrial myocardium during cardiac ischemia and that 17 miRs showed at least a 1.5-fold change in expression after ischemia. Of the 17 miRs, 9 miRs, including miR-1, miR-21, miR-24, and miR-195, which are related to apoptosis, exhibited different expression patterns in the RIPerc group compared with the control. Using qRT-PCR and Western blotting, we demonstrated that miR-1 and miR-195 were downregulated and that their common putative target gene Bcl-2 was upregulated in the RIPerc group. However, the differences in miR-21 and miR-24 expression, together with programmed cell death 4 (PDCD4), which is the target gene of miR-21, were not significant. These findings provide some insight into the role of miRs in the cardioprotective effects induced by RIPerc.

摘要

我们之前发现,远程缺血预处理(RIPerc)在减轻心脏手术期间的心肌损伤方面是有效的。鉴于微小RNA(miRs)在缺血/再灌注(I/R)损伤和细胞凋亡中发挥着重要作用,本研究旨在探讨RIPerc是否能减少心房心肌细胞凋亡以及在瓣膜置换手术过程中涉及哪些与细胞凋亡相关的miRs。在此,我们证明了RIPerc在心脏缺血期间抑制了心房心肌细胞凋亡,并且17种miRs在缺血后表达至少有1.5倍的变化。在这17种miRs中,9种与细胞凋亡相关的miRs,包括miR-1、miR-21、miR-24和miR-195,与对照组相比在RIPerc组中表现出不同的表达模式。通过qRT-PCR和蛋白质印迹法,我们证明了在RIPerc组中miR-1和miR-195表达下调,而它们共同的假定靶基因Bcl-2表达上调。然而,miR-21和miR-24的表达差异以及作为miR-21靶基因的程序性细胞死亡4(PDCD4)的差异并不显著。这些发现为miRs在RIPerc诱导的心脏保护作用中的作用提供了一些见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c1bb/4704063/c4c8ebac03b0/srep18959-f1.jpg

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