MicroRNA-200a represses myocardial infarction-related cell death and inflammation by targeting the Keap1/Nrf2 and β-catenin pathways.

Hellenic Journal of Cardiology : HJC = Hellēnikē Kardiologikē Epitheōrēsē
Yi MaYong Zhang

Abstract

Acute myocardial infarction (MI) is a main cause of emergency death in the world. MicroRNAs (miRs/miRNAs) are a series of small non-coding RNA molecules, which regulate cardiovascular disorders that involve MI. In this study, we explored the function of miR-200a in MI treatment. We observed down-regulation of miR-200a levels and up-regulation of Keap1 and β-catenin levels in H2O2-treated newborn murine ventricular cardiomyocytes (NMVCs) and the infarcted heart tissues of MI mouse models, compared to the non-treated NMVCs and normal heart tissues of healthy mice. CCK-8 and colony formation assays indicated the reduction in NMVC vitality due to H2O2 treatment and the recovery of cell vitality due to miR-200a overexpression, respectively. Flow cytometry with Annexin and PI staining indicated the inhibition of H2O2-triggered cell apoptosis through ectopically expressed miR-200a. Western blotting and ELISA analyses that detected pro-inflammatory cell factors [interleukin (IL)-1β, IL-6, and tumor necrosis factor (TNF)-α] confirmed that miR-200a prevented H2O2-induced NMVC inflammation. Moreover, miR-200a inhibited up-regulation of Keap1 and β-catenin expression in H2O2-treated NMVCs by directly binding with the 3'-UTR regions of both...Continue Reading

References

Mar 1, 1973·The Journal of Clinical Investigation·P LibbyE Braunwald
May 18, 2001·American Journal of Physiology. Heart and Circulatory Physiology·E PalojokiI Tikkanen
Dec 18, 2001·Cardiovascular Research·Nikolaos G FrangogiannisMark L Entman
Jun 20, 2006·The International Journal of Biochemistry & Cell Biology·Antonio AbbateAlfonso Baldi
Oct 29, 2008·Genome Research·Robin C FriedmanDavid P Bartel
Aug 27, 2009·The Journal of Biological Chemistry·Shimin DongChunxiang Zhang
Oct 21, 2010·Physiological Genomics·Yumei YeYochai Birnbaum
Aug 13, 2011·Hepatology : Official Journal of the American Association for the Study of Liver Diseases·Ji-hang YuanShu-han Sun
Dec 23, 2011·Cell Death & Disease·M ChiongS Lavandero
Jan 6, 2012·The New England Journal of Medicine·Elizabeth G Nabel, Eugene Braunwald
May 23, 2012·Cellular Physiology and Biochemistry : International Journal of Experimental Cellular Physiology, Biochemistry, and Pharmacology·Zhihua LiuXiaobo Sun
Jan 24, 2013·Clinical Cancer Research : an Official Journal of the American Association for Cancer Research·San-Jian YuZhi-Ming Shao
Aug 5, 2016·International Journal of Biological Sciences·Pengzhou HangZhimin Du
Apr 5, 2017·Toxicology and Applied Pharmacology·Joshua Strom, Qin M Chen
Feb 8, 2020·The Journal of Endocrinology·Ziping JiangHao Wu

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Citations

Mar 21, 2021·Free Radical Biology & Medicine·Changhai TianIrving H Zucker

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