BCL-2 delay apoptosis and PARP cleavage induced by NO donors in GT1-7 cells.
BCL-2 is a negative regulator of cell death in several systems. Here we report that bcl-2 expression protects against apoptosis induced by nitric oxide (NO) donors in GT1-7 hypothalamic cells. BCL-2 significantly inhibited neuronal death caused by 200 microM S-nitroso-cysteine (SNOC), 200 microM S-nitroso-N-acetyl-penicillamine (SNAP), or 1 mM 3-morpholinosydnonimine (SIN-1). To explore further the protective mechanism(s) elicited by bcl-2 expression, we investigated whether BCL-2 could prevent NO-induced cleavage of poly-ADP-ribose-polymerase (PARP), which is a substrate for interleukin-1 beta 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.
Bonfoco
E
E
Institute of Environmental Medicine, Karolinska Institutet, Stockholm, Sweden.
Zhivotovsky
B
B
Rossi
A D
AD
Aguilar-Santelises
M
M
Orrenius
S
S
Lipton
S A
SA
Nicotera
P
P
D017209:Apoptosis / Q000502:physiology*; D015153:Blotting, Western; D002460:Cell Line; D002467:Cell Nucleus / Q000502:physiology / Q000648:ultrastructure; D053938:DNA Fragmentation; D005434:Flow Cytometry; D015870:Gene Expression / Q000502:physiology; D019254:Genes, bcl-2 / Q000502:physiology*; D006801:Humans; D007031:Hypothalamus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D009474:Neurons / Q000187:drug effects / Q000201:enzymology / Q000378:metabolism; D009569:Nitric Oxide / Q000494:pharmacology*; D011065:Poly(ADP-ribose) Polymerases / Q000378:metabolism*
D009569:Nitric Oxide; D011065:Poly(ADP-ribose) Polymerases