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miR-130 aggravates acute myocardial infarction-induced myocardial injury by targeting PPAR-γ

Xianglin Chu1, Yiqing Wang1, Liewen Pang1

  • 1Department of Cardiothoracic Surgery, Huashan Hospital, Fudan University, Shanghai, China.

Journal of Cellular Biochemistry
|May 16, 2018
PubMed

Insights

Downregulating miR-130 alleviates myocardial injury after infarction by increasing peroxisome proliferator-activated receptor γ (PPAR-γ) expression. This reduces inflammation and fibrosis, offering a potential therapeutic strategy for acute myocardial infarction (AMI).

Area of Science:

  • Cardiovascular Biology
  • Molecular Medicine
  • MicroRNA Therapeutics

Background:

  • Cardiac remodeling is a key pathological change following acute myocardial infarction (AMI).
  • MicroRNAs are critical posttranscriptional regulators influencing myocardial tissue post-AMI.
  • The specific role of miR-130 in AMI pathogenesis requires further elucidation.

Purpose of the Study:

  • To investigate the role and mechanism of miR-130 in acute myocardial infarction (AMI).
  • To explore the potential of targeting miR-130 for therapeutic intervention in myocardial injury.

Main Methods:

  • Utilized H9c2 cells under hypoxia to simulate myocardial infarction.
  • Employed RT-PCR, Western blot, and ELISA to assess miR-130's effects.
  • Verified miR-130 targets using bioinformatics and luciferase reporter assays.
  • Confirmed findings in a rat model of induced myocardial injury.

Main Results:

  • miR-130 downregulation reduced hypoxia-induced inflammation and fibrosis in H9c2 cells.
  • miR-130 inhibition reversed hypoxia-induced suppression of peroxisome proliferator-activated receptor γ (PPAR-γ).
  • PPAR-γ was confirmed as a direct target of miR-130, mediating cardioprotection by inhibiting NFκB and TGF-β1.
  • In vivo studies showed miR-130 knockdown enhanced PPAR-γ's protective effects against myocardial injury.

Conclusions:

  • miR-130 knockdown alleviates infarction-induced myocardial injury.
  • The mechanism involves promoting PPAR-γ expression, which suppresses inflammation and fibrosis.
  • Targeting miR-130 represents a promising therapeutic strategy for acute myocardial infarction.
Keywords:
PPAR-γacute myocardial infarctioninflammationmiR-130myocardial fibrosis

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