BCL-2 DELAY APOPTOSIS AND PARP CLEAVAGE INDUCED BY NO DONORS IN GT1-7CELLS

BCL-2 is a negative regulator of cell death in several systems. Here w e report that bcl-2 expression protects against apoptosis induced by n itric oxide (NO) donors in GT1-7 hypothalamic cells. BCL-2 significant ly inhibited neuronal death caused by 200 mu M S-nitrosocysteine (SNOC ), 200 mu M S-nitroso-N-acetyl-penicillamine (SNAP), or 1 mM 3-morphol inosydnonimine (SIN-1). To explore further the protective mechanism(s) elicited by bcl-2 expression, we investigated whether BCL-2 could pre vent NO-induced cleavage of poly-ADP-ribose-polymerase (PARP), which i s a substrate for interleukin-1 beta converting enzyme (ICE)-like prot eases in apoptosis. Formation of 85 and 25 kDa PARP fragments elicited by NO donors was inhibited in cells over-expressing bcl-2.