The proto-oncogene bcl-2 can selectively rescue neurotrophic factor-dependent neurons from apoptosis

Apoptosis as a mechanism of neuronal cell death following acute experimental spinal cord injury

“…Various antiapoptotic agents have been shown to limit apoptotic cell death and may therefore limit neural tissue death in the zone of spinal cord injury. 19,23 One such anti-apoptotic agent, the oncogene Bcl-2, has already been shown to improve histologic survival following an acute experimental spinal cord injury in the rat model. 24 Bcl-2 overexpression was produced invivo following introduction of the Bcl-2 gene via a recombinant adenovirus vector prior to the same experimental spinal cord injury administered in this study.…”

“…However, the knowledge of apoptosis occurring following acute spinal cord injury could prove to be an important avenue for improved neuronal cell survival by blocking or limiting apoptotic cell death, which has been shown possible in a variety of tissues. 19,20 Recently, the ability to accurately determine apoptotic cell death has become available using the TUNEL assay. This provides in situ labeling of internucleosomally degraded DNA which is the hallmark of apoptotic cell death.…”

Bcl-2, Bcl-xL and adenovirus protein E1B19kD are functionally equivalent in their ability to inhibit cell death

“…Moreover, although bcl-2 transgene expression enhances the survival of immature B and T cells that have failed to receive a survival signal (`death by neglect') (Linette et al, 1994;Strasser et al, 1994b,c), it is an ine ective antidote to`activation induced apoptosis' of lymphocytes bearing autoreactive antigen receptors (Sentman et al, 1991;Strasser et al, , 1994b and does not protect against killing mediated by cytotoxic T cells (Vaux et al, 1992b). This inability of Bcl-2 to antagonise all pathways to physiological cell death is not restricted to lymphocytes, since its overexpression enhances the survival of sensory neurons deprived of NGF, but does not prevent apoptosis of ciliary neurons deprived of ciliary neurotrophic factor (CNTF) (Allsopp et al, 1993).…”

Inhibition of Bcl-xL expression sensitizes normal human keratinocytes and epithelial cells to apoptotic stimuli

“…Its oncogenic potential has been shown to result from the inhibition of apoptotic cell death (McDonnell and Korsmeyer, 1991). Both Bcl-2 and the related gene family member Bcl-x L have been shown to be potent inhibitors of a wide variety of apoptotic stimuli (Allsopp et al, 1993;Strasser et al, 1991;Miyashita and Reed, 1992;Ohmori et al, 1993;Walton et al, 1993). Genetic knockout studies of Bcl-2 and Bcl-x L have demonstrated the necessity of these proteins to prevent apoptosis and to allow for proper organ development in the mouse (Veis et al, 1993;Motoyama et al, 1995).…”