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The bcl-2 gene product prevents programmed cell death of ventricular myocytes

L A Kirshenbaum1, D de Moissac

  • 1Institute of Cardiovascular Sciences, St Boniface General Hospital Research Centre, Department of Physiology, Faculty of Medicine, University of Manitoba, Winnipeg, Canada. Lorrie@SBRC.umanitoba.ca

Circulation
|October 7, 1997
PubMed
Abstract

Insights

The antiapoptotic protein bcl-2 prevents programmed cell death in cardiac muscle cells triggered by p53. This study demonstrates bcl-2

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cell Death Research

Background:

  • Programmed cell death (apoptosis) is crucial in cardiac muscle.
  • p53 is a known inducer of apoptosis across various cell types.
  • The role of bcl-2 in preventing cardiac myocyte apoptosis requires investigation.

Purpose of the Study:

  • To determine if the antiapoptotic protein bcl-2 can prevent p53-induced apoptosis in cardiac muscle cells (ventricular myocytes).

Main Methods:

  • Utilized replication-defective adenovirus to deliver bcl-2 and p53 genes into ventricular myocytes.
  • Assessed myocyte cell death using vital staining.
  • Evaluated apoptosis via DNA fragmentation and terminal transferase deoxynucleotide end labeling.
  • Measured bax promoter transcription levels.

Main Results:

  • p53 significantly increased ventricular myocyte death and apoptosis.
  • p53 also increased bax promoter transcription.
  • bcl-2 expression prevented p53-induced myocyte death and apoptosis.
  • bcl-2 repressed p53-dependent bax transcription.

Conclusions:

  • bcl-2 functions as an antiapoptotic factor in ventricular myocytes.
  • This is the first evidence of bcl-2's antiapoptotic role in cardiac muscle cells.
  • bcl-2's protective effect is linked to the repression of p53-mediated bax transcription.

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