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Transforming growth factor-beta(1) induces apoptosis via connective tissue growth factor in human aortic smooth

K Hishikawa1, T Nakaki, T Fujii

  • 1Department of Pharmacology, Teikyo University School of Medicine, Kaga 2-11-1, Itabashi-ku, Tokyo, Japan. hisikawa@med.teikyo-u.ac.jp

European Journal of Pharmacology
|December 23, 1999
PubMed

Insights

Transforming growth factor-beta(1) (TGF-beta(1)) triggers apoptosis in human aortic smooth muscle cells via connective tissue growth factor (CTGF). Inhibiting CTGF reversed TGF-beta(1)-induced cell death and caspase activation.

Area of Science:

  • Cardiovascular Biology
  • Cellular Signaling
  • Molecular Medicine

Background:

  • Transforming growth factor-beta(1) (TGF-beta(1)) is implicated in vascular remodeling and disease.
  • Apoptosis in vascular smooth muscle cells contributes to cardiovascular pathologies.
  • Connective tissue growth factor (CTGF) is a key mediator in tissue repair and fibrosis.

Purpose of the Study:

  • To investigate the role of CTGF in TGF-beta(1)-induced apoptosis in human aortic vascular smooth muscle cells (HASC).

Main Methods:

  • HASC were treated with TGF-beta(1) to induce apoptosis.
  • CTGF mRNA and protein levels were assessed.
  • The effect of a CTGF antisense oligonucleotide on TGF-beta(1) effects was evaluated.
  • Cell viability, DNA fragmentation, and caspase 3 activation were measured.

Main Results:

  • TGF-beta(1) significantly increased CTGF mRNA and protein expression in HASC.
  • A CTGF antisense oligonucleotide attenuated TGF-beta(1)-induced reduction in cell viability and DNA fragmentation.
  • The CTGF antisense oligonucleotide inhibited TGF-beta(1)-induced caspase 3 activation.

Conclusions:

  • CTGF is a critical mediator in the process of TGF-beta(1)-induced apoptosis in human aortic vascular smooth muscle cells.
  • Targeting CTGF may represent a therapeutic strategy for cardiovascular diseases involving TGF-beta(1) signaling.

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