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Related Experiment Video

Updated: May 12, 2026

A Novel Stretching Platform for Applications in Cell and Tissue Mechanobiology
16:46

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Published on: June 3, 2014

Mechanical stretch changes coronary artery fibroblasts function by upregulating HSF1 protein expression.

Jiming Li1, Yibo Zhang, Li Cui

  • 1Department of Cardiology, East Hospital, Tongji University School of Medicine, Shanghai 200120, China. lxb70@hotmail.com

International Journal of Biological Macromolecules
|April 2, 2013
PubMed
Summary

Mechanical stretch enhances fibroblast proliferation and collagen production. This process may involve the upregulation of Heat Shock Factor 1 (HSF1) expression, influencing cellular function and inflammatory responses.

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Area of Science:

  • Cardiovascular Biology
  • Cellular Mechanotransduction

Background:

  • Fibroblast cells play a crucial role in tissue repair and remodeling.
  • Mechanical forces are increasingly recognized as significant regulators of cellular behavior in cardiovascular tissues.

Purpose of the Study:

  • To investigate the impact of mechanical stretch on human coronary artery fibroblast function.
  • To elucidate the molecular mechanisms underlying these changes, particularly the role of HSF1.

Main Methods:

  • Cell culture of human coronary artery fibroblasts.
  • Application of mechanical stretch (24h) to a subset of cells.
  • Assays for proliferation (CCK-8), collagen secretion (ELISA, Hydroxyproline), and gene expression (RT-PCR) of MMP, TIMP, IL-6, alpha-SMA, HSF1, HSP70.
  • Protein expression analysis of HSF1 (Western-blotting).

Main Results:

  • Mechanical stretch significantly increased fibroblast proliferation and collagen secretion.
  • Upregulation of MMP-9/TIMP ratio, alpha-SMA, IL-6, HSF1, and HSP70 mRNA was observed in the stretch group.
  • Western-blotting confirmed increased HSF1 protein expression under mechanical stretch.

Conclusions:

  • Mechanical stretch alters human coronary artery fibroblast proliferation and collagen formation.
  • The observed changes in cellular function and inflammatory factor secretion are potentially mediated by the upregulation of HSF1 protein expression.