Cited by 368MicroRNA in disease regulationCardiac Ischemia and ReperfusionCardiac Fibrosis and Remodeling

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MicroRNA-21 protects against the H2O2-induced injury on cardiac myocytes via its target gene PDCD4

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Cheng, Yunhui, Liu, Xiaojun, Zhang, Shuo, Lin, Ying, Yang, Jian, Zhang, Chunxiang·2009·Journal of Molecular and Cellular Cardiology

DOI 10.1016/j.yjmcc.2009.01.008PMC PMC3593965

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Abstract

Reactive oxygen species (ROS)-induced cardiac cell injury via expression changes of multiple genes plays a critical role in the pathogenesis of numerous heart diseases. MicroRNAs (miRNAs) comprise a novel class of endogenous, small, noncoding RNAs that negatively regulate about 30% of the genes in a cell via degradation or translational inhibition of their target mRNAs. Currently, the effects of ROS on miRNA expression and the roles of miRNAs in ROS-mediated injury on cardiac myocytes are uncertain. Using quantitative real-time RT-PCR (qRT-PCR), we demonstrated that microRNA-21 (miR-21) was upregulated in cardiac myocytes after treatment with hydrogen peroxide (H2O2). To determine the potential roles of miRNAs in H2O2-mediated gene regulation and cellular injury, miR-21 expression was downregulated by miR-21 inhibitor and upregulated by pre-miR-21. H2O2-induced cardiac cell death and apoptosis were increased by miR-21 inhibitor and was decreased by pre-miR-21. Programmed cell death 4 (PDCD4) that was regulated by miR-21 and was a direct target of miR-21 in cardiac myocytes. Pre-miR-21-mediated protective effect on cardiac myocyte injury was inhibited in H2O2-treated cardiac cells via adenovirus-mediated overexpression of PDCD4 without miR-21 binding site. Moreover, Activator protein 1 (AP-1) was a downstream signaling molecule of PDCD4 that was involved in miR-21-mediated effect on cardiac myocytes. The results suggest that miR-21 is sensitive to H2O2 stimulation. miR-21 participates in H2O2-mediated gene regulation and functional modulation in cardiac myocytes. miR-21 might play an essential role in heart diseases related to ROS such as cardiac hypertrophy, heart failure, myocardial infarction, and myocardial ischemia/reperfusion injury.

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Authors: Cheng, Y., Liu, X., Zhang, S., Lin, Y., Yang, J., & Zhang, C.
Affiliations: Rutgers New Jersey Medical School (US)
Corresponding author: Zhang, Chunxiang
ORCID: Liu, Xiaojun
Zhang, Shuo
Lin, Ying
Yang, Jian
Zhang, Chunxiang
Venue: Journal of Molecular and Cellular Cardiology
Publisher: Elsevier BV
Published: 2009-07
Volume: 47
Issue: 1
Pages: 5-14
ISSN: 0022-2828 (ISSN-L)
DOI: 10.1016/j.yjmcc.2009.01.008
PMC: PMC3593965
OpenAlex: W2141570739
Semantic Scholar: 1fbe4e1a56db9230d95dce535ef1d9e12a4d760a
Cited by: 368
References: 36
Citations by year: 2026: 8 · 2025: 9 · 2024: 14 · 2023: 11 · 2022: 16 · 2021: 20 · 2020: 24 · 2019: 25 · 2018: 23 · 2017: 18 · 2016: 29 · 2015: 23 · 2014: 26 · 2013: 28 · 2012: 29
FWCI: 10.27
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations: Journal of Molecular and Cellular Cardiology (publishedVersion)
PubMed (publishedVersion)
Europe PMC (PubMed Central) (acceptedVersion)
PubMed Central (acceptedVersion)
Funders: National Institutes of Health
National Heart, Lung, and Blood Institute (HL 080133, R01HL095707, R01HL080133)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Ischemia and Reperfusion
Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Cardiac Fibrosis and Remodeling
Keywords: miR-21, PDCD4, hydrogen peroxide, reactive oxygen species, cardiomyocytes, oxidative stress, apoptosis, cardioprotection, AP-1, microRNA target regulation, heart disease
MeSH terms: Animals, Hydrogen Peroxide, Necrosis, Blotting, Western, Rats, Sprague-Dawley, Apoptosis, Transcription Factor AP-1, Reverse Transcriptase Polymerase Chain Reaction, Myocytes, Cardiac, MicroRNAs, Apoptosis Regulatory Proteins, Rats

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MicroRNA-21 protects against the H2O2-induced injury on cardiac myocytes via its target gene PDCD4

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