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Updated: Aug 9, 2026

Development of an In Vitro Assay to Evaluate Contractile Function of Mesenchymal Cells that Underwent Epithelial-Mesenchymal Transition
06:02

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Connective tissue growth factor is responsible for transforming growth factor-beta-induced peritoneal mesothelial

Cheuk-Chun Szeto1, Kai-Ming Chow, Ka-Bik Lai

  • 1Department of Medicine, Prince of Wales Hospital, The Chinese University of Hong Kong, Shatin, Hong Kong, SAR, China. ccszeto@cuhk.edu.hk

Nephron. Experimental Nephrology
|April 26, 2006
PubMed
Abstract

Insights

Connective tissue growth factor (CTGF) mediates transforming growth factor-beta (TGF-beta)-induced apoptosis in peritoneal mesothelial cells (PMC). Blocking CTGF with siRNA prevents TGF-beta-induced PMC apoptosis, highlighting CTGF as a key downstream mediator.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Renal Physiology

Background:

  • Transforming growth factor-beta (TGF-beta) stimulates peritoneal mesothelial cells (PMC) to produce connective tissue growth factor (CTGF).
  • High doses of TGF-beta can induce apoptosis in PMC.
  • CTGF is potentially a downstream mediator of TGF-beta's effects.

Purpose of the Study:

  • To investigate the role of CTGF in TGF-beta-induced apoptosis of PMC.
  • To determine if CTGF blockade can prevent TGF-beta-induced PMC apoptosis.

Main Methods:

  • Primary culture of rat PMC.
  • Flow cytometry to assess apoptosis.
  • CTGF blockade using antibodies and short-interfering RNA (siRNA).
  • Real-time polymerase chain reaction to analyze apoptotic gene expression (BAX, BCL-2L).

Main Results:

  • TGF-beta upregulated BAX and downregulated BCL-2L, increasing PMC apoptosis fourfold.
  • Antibody-mediated CTGF blockade partially prevented TGF-beta-induced apoptosis.
  • CTGF-specific siRNA completely abolished TGF-beta-induced PMC apoptosis, without affecting necrosis.
  • CTGF silencing prevented TGF-beta-induced downregulation of BCL-2L but not BAX expression.

Conclusions:

  • CTGF is a critical downstream mediator in the pathway of TGF-beta-induced PMC apoptosis.
  • Targeting CTGF may represent a therapeutic strategy for conditions involving TGF-beta-mediated mesothelial cell apoptosis.

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