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Examining BCL-2 Family Function with Large Unilamellar Vesicles
08:35

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

Bax is not the heterodimerization partner necessary for sustained anti-photoreceptor-cell-death activity of Bcl-2

Pamela Eversole-Cire1, Jeannie Chen, Melvin I Simon

  • 1Division of Biology, California Institute of Technology, Pasadena, CA 91125, USA.

Investigative Ophthalmology & Visual Science
|May 1, 2002
PubMed
Abstract

Insights

Co-expressing Bcl-2 and Bax in photoreceptors did not improve the temporary protective effect against retinal degeneration in a mouse model of autosomal dominant retinitis pigmentosa (adRP). This suggests that combining these proteins does not offer enhanced neuroprotection for RP.

Area of Science:

  • Ophthalmology
  • Neuroscience
  • Genetics

Background:

  • Bcl-2 protein can temporarily slow retinal degeneration in mouse models of retinitis pigmentosa (RP).
  • The temporary effect of Bcl-2 may be due to insufficient functional complexes with other proteins.
  • Bax protein typically induces apoptosis but can be anti-apoptotic when complexed with Bcl-2.

Purpose of the Study:

  • To determine if coexpressing Bcl-2 and Bax enhances the neuroprotective effect in photoreceptors of autosomal dominant retinitis pigmentosa (adRP) mouse models.
  • To investigate the potential synergistic effects of Bcl-2 and Bax in preventing photoreceptor cell death.

Main Methods:

  • Generated transgenic mice with photoreceptor-specific overexpression of Bax and Bcl-2 using the murine opsin promoter.
  • Crossed these transgenic mice with an adRP mouse model.
  • Performed morphologic analysis of retinas at various developmental stages to track disease progression.

Main Results:

  • Photoreceptor-specific Bax overexpression led to significant rod cell death, dependent on transgene expression levels.
  • Bcl-2 inhibited Bax-induced photoreceptor cell death.
  • Coexpression of Bcl-2 and Bax did not improve the neuroprotective effect beyond that of Bcl-2 alone in adRP mice.

Conclusions:

  • Coexpression of Bax and Bcl-2, at the levels achieved in these transgenic lines, does not prolong the temporary neuroprotective effect of Bcl-2 in adRP mouse photoreceptors.
  • The combination of Bcl-2 and Bax does not offer enhanced protection against retinal degeneration in this model.

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