Abstract
Antiapoptotic members of the Bcl-2 family have been shown to reduce ischemic brain injury in vivo and in vitro. Understanding early changes in respiration are important in understanding the cells response to stress and the mechanisms of protection afforded by overexpression of protective genes. This mini-review summarizes current knowledge regarding early responses of astrocytes to ischemia-like stress and the effects of overexpression of protective Bcl-2 family genes on astrocyte mitochondrial function. Overexpression of Bcl-x(L) improves mitochondrial respiratory function, normalizes mitochondrial membrane potential, and reduces production of free radicals early after the imposition of a stress in primary cultured murine astrocytes.
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