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Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis.

ABSTRACT: Prostaglandin-E1 (PGE1) is a potent vasodilator with anti-inflammatory and antiplatelet effects. However, the mechanism by which PGE1 contributes to the amelioration of cardiac injury remains unclear. The present study was designed to investigate how PGE1 protects against hypoxia/reoxygenation (H/R)-induced injuries by regulating microRNA-21-5p (miR-21-5p) and fas ligand (FASLG). Rat H9C2 cells and isolated primary cardiomyocytes were cultured under hypoxic conditions for 6 h (6H, hypoxia for 6 h), and reoxygenated for periods of 6 (6R, reoxygenation for 6 h), 12, and 24 h, respectively. Cells from the 6H/6R group were treated with various doses of PGE1; after which, their levels of viability and apoptosis were detected. The 6H/6R treatment regimen induced the maximum level of H9C2 cell apoptosis, which was accompanied by the highest levels of Bcl-2-associated X protein (Bax) and cleaved-caspase-3 expression and the lowest level of B-cell lymphoma 2 (Bcl-2) expression. Treatment with PGE1 significantly diminished the cell cytotoxicity and apoptosis induced by the 6H/6R regimen, and also decreased expression of IL-2, IL-6, P-p65, TNF-α, and cleaved-caspase-3. In addition, we proved that PGE1 up-regulated miR-21-5p expression in rat cardiomyocytes exposed to conditions that produce H/R injury. FASLG was a direct target of miR-21-5p, and PGE1 reduced the ability of H/R-injured rat cardiomyocytes to undergo apoptosis by affecting the miR-21-5p/FASLG axis. In addition, we proved that PGE1 could protect primary cardiomyocytes against H/R-induced injuries. These results indicate that PGE1 exerts cardioprotective effects in H9C2 cells during H/R by regulating the miR-21-5p/FASLG axis.

SUBMITTER: Tang M

PROVIDER: S-EPMC6923339 | biostudies-literature | 2019 Dec

REPOSITORIES: biostudies-literature

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Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis.

Tang Mingxiang M Pan Hongwei H Zheng Zhaofen Z Guo Yin Y Peng Jianqiang J Yang Jun J Luo Yangping Y He Jin J Yan Sulan S Wang Peng P Zhang Yi Y Zhou Yulu Y

Bioscience reports 20191201 12

<h4>Background</h4>Prostaglandin-E1 (PGE1) is a potent vasodilator with anti-inflammatory and antiplatelet effects. However, the mechanism by which PGE1 contributes to the amelioration of cardiac injury remains unclear.<h4>Methods</h4>The present study was designed to investigate how PGE1 protects against hypoxia/reoxygenation (H/R)-induced injuries by regulating microRNA-21-5p (miR-21-5p) and fas ligand (FASLG). Rat H9C2 cells and isolated primary cardiomyocytes were cultured under hypoxic cond ...[more]

PMID: 31782491

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Project description:Icariside II (ICS II) has been reported to have protective effects against oxidative stress. However, whether ICS II protects cardiomyocytes from myocardial infarction (MI), and the associated underlying mechanisms, remain to be elucidated. Therefore, the current study investigated the effects of ICS II on hypoxia?injured H9c2 cells, as well as the associated molecular mechanisms. A hypoxic injury model was established to emulate the effects of MI. The effects of ICS II on the proliferation of rat cardiomyocyte H9c2 cells were assessed with cell counting kit?8 assays. The apoptotic status of the cells was assessed by flow cytometry, and the expression of apoptosis?related proteins was analyzed by western blotting. A microRNA (miRNA/miR) microarray was used to quantify the differential expression of miRNAs after ICS II treatment, and the levels of miR?7?5p were further quantified by reverse transcription?quantitative PCR. Whether ICS II affected hypoxia?injured cells via miR?7?5p was subsequently examined, and the target of miR?7?5p was also investigated by bioinformatics analysis and luciferase reporter assays. The effects of ICS II on the PI3K/Akt pathway were then evaluated by western blot analysis. Hypoxia treatment decreased viability and the migration and invasion abilities of H9c2 cells, and also induced apoptosis. ICS II significantly increased viability and reduced hypoxia?associated apoptosis. Moreover, ICS II treatment led to the upregulation of miR?7?5p, and the protective effects of ICS II were found to rely on miR?7?5p. Moreover, BTG anti?proliferation factor (BTG2) was identified as a direct target of miR?7?5p, and overexpression of BTG2 inhibited the protective effects of miR?7?5p. Finally, ICS II treatment resulted in the activation of the PI3K/Akt signaling pathway, which is essential for the survival of H9c2 cells under hypoxic conditions. In summary, ICS II reduces hypoxic injury in H9c2 cells via the miR?7?5p/BTG2 axis and activation of the PI3K/Akt signaling pathway.

Dataset Information

Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis.

Publications

Prostaglandin E1 protects cardiomyocytes against hypoxia-reperfusion induced injury via the miR-21-5p/FASLG axis.

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