Bcl-2 family gene products in cerebral ischemia and traumatic brain injury.
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.
Graham
S H
SH
Department of Neurology, University of Pittsburgh School of Medicine, Pennsylvania, USA. sgra+@pitt.edu
Chen
J
J
Clark
R S
RS
D000818:Animals; D017209:Apoptosis / Q000235:genetics*; D001930:Brain Injuries / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D002545:Brain Ischemia / Q000235:genetics* / Q000378:metabolism / Q000503:physiopathology; D019254:Genes, bcl-2 / Q000502:physiology; D006801:Humans; D000090063:Proto-Oncogene Mas; D019253:Proto-Oncogene Proteins c-bcl-2 / Q000235:genetics* / Q000378:metabolism*
C000715470:MAS1 protein, human; D000090063:Proto-Oncogene Mas; D019253:Proto-Oncogene Proteins c-bcl-2