Affordable Access

deepdyve-link
Publisher Website

miR-19a mitigates hypoxia/reoxygenation-induced injury by depressing CCL20 and inactivating MAPK pathway in human embryonic cardiomyocytes.

Authors
  • Fu, Qiang1
  • Mo, Tao-Ran2
  • Hu, Xiao-Yang1
  • Fu, Yin1
  • Li, Ji3
  • 1 Department of Chinese Formulae, Heilongjiang University of Chinese Medicine, No. 24, Heping Road, Xiangfang District, Harbin, 150040, Heilongjiang, China. , (China)
  • 2 Department of Nephrology, The First Affiliated Hospital of Heilongjiang University of Traditional Chinese Medicine, Harbin, 150040, Heilongjiang, China. , (China)
  • 3 Department of Chinese Formulae, Heilongjiang University of Chinese Medicine, No. 24, Heping Road, Xiangfang District, Harbin, 150040, Heilongjiang, China. [email protected] , (China)
Type
Published Article
Journal
Biotechnology Letters
Publisher
Springer-Verlag
Publication Date
Feb 01, 2021
Volume
43
Issue
2
Pages
393–405
Identifiers
DOI: 10.1007/s10529-020-03045-2
PMID: 33165673
Source
Medline
Keywords
Language
English
License
Unknown

Abstract

Myocardial infarction (MI) is a prevalent cardiovascular puzzle and a mainspring of disease-induced mortality. We performed this investigation to detect the role of putative important miRNAs or genes in MI. CCL20 may be a potential therapeutic target, which was directly targeted and negatively regulated by miR-19a. CCL20 expression was significantly increased in MI tissue samples, but miR-19a was expressed at lower levels in MI. H/R treatment inhibited cell viability and induced an increase of apoptotic rate compared with Sham group. However, miR-19a mimic relieved the H/R-stimulated injury to cardiomyocytes. Protective effect of miR-19a against H/R in cardiomyocytes was reversed by CCL20 enhancement, and MAPK pathway was inactivated during this progression. miR-19a eliminates the H/R-induced injury in cardiomyocytes through directly targeting CCL20 and attenuating the activity of MAPK signaling pathway. These observations highlighted the therapeutic roles of miR-19a and CCL20 for MI treatment.

Report this publication

Statistics

Seen <100 times