BCL2 delay apoptosis and PARP cleavage induced by NO donors in GT17 cells

BCL-2 is a negative regulator of cell death in several systems. Here we report that bcl-2expression protects against apoptosis induced by nitric oxide (NO) donors in GT1-7 hypothalamic cells. BCL-2 significantly inhibited neuronal death caused by 200 mM S-nitrosocysteine (SNOC), 200 mM S-nitroso-N-acetyl-penicillamine (SNAP), or 1 mM 3-morpholinosydnonimine (SIN-1). To explore further the protective mechanism(s) elicited by bcl-2expression, we investigated whether BCL-2 could prevent NO-induced cleavage of poly- ADP-ribose-polymerase (PARP), which is a substrate for interleukin-1b converting enzyme (ICE)-like proteases in apoptosis. Formation of 85 and 25 kDa PARP fragments elicited by NO donors was inhibited in cells over-expressing bcl-2.