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Suppression of Pro-fibrotic Signaling Potentiates Factor-mediated Reprogramming of Mouse Embryonic Fibroblasts into Induced Cardiomyocytes
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Hepatocyte growth factor regulates the TGF-β1-induced proliferation, differentiation and secretory function of

Xin Yi1, Xiaoyan Li1, Yanli Zhou1

  • 1Department of Cardiology, Renmin Hospital of Wuhan University and Cardiovascular Research Institute of Wuhan University, Wuhan, Hubei 430060, P.R. China.

International Journal of Molecular Medicine
|May 21, 2014
PubMed

Insights

Hepatocyte growth factor (HGF) inhibits cardiac fibroblast proliferation and transformation, key drivers of cardiac fibrosis. HGF activates the c-Met-Akt-TGIF pathway, offering a potential therapeutic target for heart conditions.

Area of Science:

  • Cardiovascular Biology
  • Cellular Biology
  • Fibrosis Research

Background:

  • Cardiac fibroblast (CF) proliferation and myofibroblast transformation are central to cardiac fibrosis and pathological myocardial remodeling.
  • Transforming growth factor-β1 (TGF-β1) is a known inducer of these fibrotic processes.

Purpose of the Study:

  • To investigate the role of hepatocyte growth factor (HGF) as a regulator of cardiac fibroblast behavior in response to TGF-β1.
  • To elucidate the underlying molecular mechanisms by which HGF influences cardiac fibroblast activation.

Main Methods:

  • Assessing HGF expression levels in CFs treated with TGF-β1.
  • Modulating HGF levels (overexpression and knockdown) in CFs.
  • Evaluating CF proliferation, transformation (α-smooth muscle actin, collagen I/III expression), and secretory function.
  • Analyzing the phosphorylation of c-Met, Akt, and TGIF protein.

Main Results:

  • HGF expression decreased in CFs upon TGF-β1 treatment.
  • HGF overexpression suppressed TGF-β1-induced CF proliferation, transformation, and secretion, reducing α-SMA and collagen I/III levels.
  • HGF knockdown exacerbated TGF-β1-induced CF activation.
  • HGF modulated the phosphorylation of c-Met, Akt, and TGIF.

Conclusions:

  • HGF acts as a negative regulator of cardiac fibroblast activation and transformation.
  • HGF exerts its antifibrotic effects by activating the c-Met-Akt-TGIF signaling pathway.
  • Targeting the HGF-c-Met-Akt-TGIF axis may represent a novel therapeutic strategy for mitigating cardiac fibrosis.

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