Affordable Access

deepdyve-link
Publisher Website

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

Authors
  • Tang, Mingxiang1
  • Pan, Hongwei1
  • Zheng, Zhaofen1
  • Guo, Yin1
  • Peng, Jianqiang1
  • Yang, Jun1
  • Luo, Yangping1
  • He, Jin1
  • Yan, Sulan1
  • Wang, Peng1
  • Zhang, Yi1
  • Zhou, Yulu2
  • 1 Department of Cardiology, Hunan Provincial People's Hospital & First Affiliated Hospital of Hunan Normal University, Changsha, Hunan, China. , (China)
  • 2 Depatment of Pharmacy, The third Xiangya Hospital of Central South University, Changsha, Hunan, China. , (China)
Type
Published Article
Journal
Bioscience Reports
Publisher
Portland Press
Publication Date
Dec 20, 2019
Volume
39
Issue
12
Identifiers
DOI: 10.1042/BSR20190597
PMID: 31782491
Source
Medline
Keywords
Language
English
License
Unknown

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. © 2019 The Author(s).

Report this publication

Statistics

Seen <100 times