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Apoptosis-related microRNA changes in the right atrium induced by remote ischemic perconditioning during valve
Qinghua Hu1, Wanjun Luo1, Lingjin Huang1
1Department of cardiovascular surgery, Xiangya Hospital, Central-South University, Changsha, Hunan, China, 410078.
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.
Insights
Remote ischemic perconditioning (RIPerc) reduces apoptosis in atrial myocardium during cardiac surgery. This cardioprotective effect involves downregulation of miR-1 and miR-195, impacting Bcl-2 expression.
Area of Science:
- Cardiology
- Molecular Biology
- Cellular Biology
Background:
- Remote ischemic preconditioning (RIPerc) attenuates myocardial injury during cardiac surgery.
- MicroRNAs (miRs) play a critical role in myocardial ischemia/reperfusion (I/R) injury and apoptosis.
Purpose of the Study:
- To investigate RIPerc's effect on atrial myocardium apoptosis during valve replacement surgery.
- To identify specific apoptosis-related miRs involved in RIPerc's cardioprotective mechanism.
Main Methods:
- Quantitative reverse transcription polymerase chain reaction (qRT-PCR) to measure miR expression.
- Western blotting to assess protein levels of target genes, including Bcl-2 and programmed cell death 4 (PDCD4).
Main Results:
- RIPerc significantly inhibited atrial myocardium apoptosis during cardiac ischemia.
- Seventeen miRs showed altered expression post-ischemia; 9 apoptosis-related miRs, including miR-1, miR-21, miR-24, and miR-195, exhibited differential expression in the RIPerc group.
- miR-1 and miR-195 were downregulated, leading to the upregulation of their target gene Bcl-2 in the RIPerc group. No significant changes were observed for miR-21, miR-24, or PDCD4.
Conclusions:
- RIPerc confers cardioprotection by reducing atrial apoptosis during cardiac surgery.
- Specific miRs, notably miR-1 and miR-195, are implicated in the anti-apoptotic effects of RIPerc, likely through modulation of Bcl-2 expression.
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