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MicroRNA-199a regulates myocardial fibrosis in rats by targeting SFRP5

M-H Chen1, J-C Liu, Y Liu

  • 1Department of Emergency Medicine, The Affiliated Hospital of Southwest Medical University, Luzhou, China. cmh6186@126.com.

European Review for Medical and Pharmacological Sciences
|May 23, 2019
PubMed
Abstract

Insights

MicroRNA-199a deficiency inhibits cardiac fibroblast proliferation and migration by targeting SFRP5, offering a protective effect against myocardial fibrosis. This finding highlights microRNA-199a

Area of Science:

  • Cardiovascular Biology
  • Molecular Cardiology
  • Fibrosis Research

Background:

  • Myocardial fibrosis impairs normal heart function.
  • MicroRNAs play critical roles in cardiac remodeling.
  • Secreted frizzled-related protein 5 (SFRP5) is implicated in fibrotic processes.

Purpose of the Study:

  • To investigate the role of microRNA-199a in regulating rat myocardial fibrosis.
  • To determine if microRNA-199a targets secreted frizzled-related protein 5 (SFRP5).

Main Methods:

  • Established an in vitro myocardial fibrosis model using isoproterenol (ISO) in cardiac fibroblasts (CFs).
  • Quantified microRNA-199a, collagen I, and α-SMA expression via qRT-PCR.
  • Assessed SFRP5 and TGF-β1 protein levels using Western blot.
  • Verified microRNA-199a and SFRP5 interaction using luciferase reporter assay.
  • Evaluated CF proliferation and migration after microRNA-199a inhibitor or SFRP5 overexpression.

Main Results:

  • ISO treatment significantly upregulated microRNA-199a in CFs.
  • MicroRNA-199a inhibition reduced CF proliferation, migration, and cardiac fibroblast-to-myofibroblast transformation (CMT).
  • Confirmed direct binding between microRNA-199a and SFRP5 3'UTR.
  • SFRP5 overexpression counteracted the effects of microRNA-199a inhibition on CFs.

Conclusions:

  • MicroRNA-199a deficiency mitigates CF proliferation, migration, and CMT by targeting SFRP5.
  • This mechanism provides a protective effect against myocardial fibrosis.
  • MicroRNA-199a emerges as a potential therapeutic target for myocardial fibrosis.

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