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MicroRNA-325 alleviates myocardial fibrosis after myocardial infarction via downregulating GLI1

C-C Wang1, B-B Shang, C-W Yang

  • 1Emergency Center, The Second Hospital of Dalian Medical University, Liaoning, China. tina2000wan@sohu.com.

European Review for Medical and Pharmacological Sciences
|September 5, 2018
PubMed
Abstract

Insights

MicroRNA-325 plays a protective role in myocardial fibrosis following myocardial infarction (MI). Upregulating microRNA-325 reduces infarct size and improves cardiac function by inhibiting GLI1 expression.

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • Biomedical Research

Background:

  • Myocardial infarction (MI) often leads to myocardial fibrosis, a significant cause of heart failure.
  • MicroRNAs (miRNAs) are emerging as critical regulators in cardiac remodeling and fibrosis.
  • The specific role of microRNA-325 in post-MI myocardial fibrosis remains largely unexplored.

Purpose of the Study:

  • To investigate the role of microRNA-325 in myocardial fibrosis after myocardial infarction (MI).
  • To elucidate the underlying molecular mechanism by which microRNA-325 influences cardiac fibrosis.
  • To assess the therapeutic potential of microRNA-325 in a rat model of MI.

Main Methods:

  • A rat model of myocardial infarction was established using left anterior descending artery ligation.
  • Quantitative real-time polymerase chain reaction (qRT-PCR) was used to measure miRNA and fibrotic marker expression.
  • In vivo lentivirus-mediated microRNA-325 upregulation and in vitro cardiac fibroblast assays were performed.
  • Echocardiography and α-SMA expression analysis assessed cardiac function and fibrosis.
  • Dual-luciferase reporter gene assays verified the interaction between microRNA-325 and GLI1.

Main Results:

  • MicroRNA-325 levels were downregulated in the infarcted cardiac tissue post-MI.
  • Overexpression of microRNA-325 significantly reduced mortality and infarct size in MI rats.
  • MicroRNA-325 upregulation improved cardiac function, evidenced by elevated LVEF and LVFS.
  • In vitro, microRNA-325 inhibited cardiac fibroblast proliferation, migration, and α-SMA expression.
  • MicroRNA-325 was found to directly inhibit the expression of GLI1.

Conclusions:

  • MicroRNA-325 is downregulated after myocardial infarction and contributes to myocardial fibrosis.
  • Overexpression of microRNA-325 exerts cardioprotective effects by alleviating myocardial fibrosis.
  • The antifibrotic mechanism involves the direct inhibition of GLI1 expression by microRNA-325.

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