Calreticulin promotes proliferation and extracellular matrix expression through Notch pathway in cardiac fibroblasts

Xiaoying Fan1, Yuan Yao1, Yao Zhang1

  • 1Department of Cardiovascular Medicine, 2nd Affiliated Hospital of Harbin Medical University, China.

Abstract

Insights

Calreticulin (CRT) overexpression in human cardiac fibroblasts increases cell viability and invasiveness, promoting cardiac fibrosis. This suggests CRT plays a key role in cardiac disease development.

Area of Science:

  • Cardiology
  • Molecular Biology
  • Cell Biology

Background:

  • Cardiac fibrosis is a major contributor to various heart diseases.
  • Calreticulin (CRT) is implicated in cardiac pathologies, with its expression levels affecting disease severity.

Purpose of the Study:

  • To investigate the impact of Calreticulin (CRT) on cardiac fibrosis.
  • To elucidate the molecular mechanisms underlying CRT's role in cardiac fibrosis.

Main Methods:

  • Human cardiac fibroblast cells (HCF) were transfected with CRT expression vectors or siRNA.
  • Cell viability, apoptosis, and invasion assays were conducted.
  • Gene and protein expression levels were analyzed using qRT-PCR and Western blot.

Main Results:

  • CRT overexpression significantly increased HCF viability and invasiveness while decreasing apoptosis.
  • CRT overexpression elevated collagen (I and III) and matrix metalloproteinase (MMP-2 and 9) levels.
  • The Notch pathway was activated by CRT overexpression and suppressed upon its reduction.

Conclusions:

  • CRT overexpression in HCF promotes fibrosis-associated characteristics like increased viability and invasiveness.
  • CRT's activation of the Notch pathway is a potential mechanism contributing to CRT-induced cardiac fibrosis.

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