Bcl-2 family gene products in cerebral ischemia and traumatic brain injury

J Neurotrauma. 2000 Oct;17(10):831-41. doi: 10.1089/neu.2000.17.831.

Abstract

The proto-oncogene bcl-2 plays a key role in regulating programmed cell death in neurons. The present review discusses the mechanisms by which bcl-2 family genes regulate programmed cell death, and their role in controlling cell death in cerebral ischemia and traumatic brain. Expression of several bcl-2 family members is altered in brain tissues after ischemia and trauma, suggesting that bcl-2 family genes could play a role in determining the fate of injured neurons. Furthermore, alteration of expression of bcl-2 family genes using transgenic approaches, viral vectors, or anti-sense oligonucleotides modifies neuronal cell death and neurological outcome after injury. These data suggest that the activity of bcl-2 family gene products participates in determining cellular and neurologic outcomes in ischemia and trauma. Strategies that either mimic the death-suppressor effects or inhibit the death-promoter effects of bcl-2 family gene products may improve outcome after ischemia and trauma.

Publication types

  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Brain Injuries / genetics*
  • Brain Injuries / metabolism
  • Brain Injuries / physiopathology
  • Brain Ischemia / genetics*
  • Brain Ischemia / metabolism
  • Brain Ischemia / physiopathology
  • Genes, bcl-2 / physiology
  • Humans
  • Proto-Oncogene Proteins c-bcl-2 / genetics*
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*

Substances

  • Proto-Oncogene Proteins c-bcl-2