bcl-2 inhibits death of central neural cells induced by multiple agents.

L T Zhong(University of California, Los Angeles), Theodore A. Sarafian(University of California, Los Angeles), Darci J. Kane(University of California, Los Angeles), Andrew Charles(University of California, Los Angeles), Steven Mah(University of California, Los Angeles), Robert H. Edwards(University of California, Los Angeles), Dale E. Bredesen(University of California, Los Angeles)
Proceedings of the National Academy of Sciences
May 15, 1993
10.1073/pnas.90.10.4533
Cited by 628Open Access

Abstract

The protooncogene bcl-2, which has been implicated in B-cell lymphoma development, inhibits apoptosis due to growth factor withdrawal in some, but not all, hematopoietic cells. Recently we found that bcl-2 also inhibits apoptosis in PC12 pheochromocytoma cells. We now report that bcl-2 inhibits the death of a central neural cell line due to serum and growth factor withdrawal, the calcium ionophore A23187, glucose withdrawal, membrane peroxidation, and, in some cases, free radical-induced damage. This broad range of protective effects of BCL-2 protein suggests that BCL-2 may interact with a central step in neural cell death. Measurements of intracellular free calcium suggest that BCL-2 alters the transduction of neural death signals at a point distal to the rise in intracellular free calcium.

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