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Nitric Oxide Suppression of Apoptosis Occurs in Association with an Inhibition of Bcl-2 Cleavage and Cytochrome cRelease*

Young-Myeong Kim,Tae-Hyoung Kim,D. Seol,R. Talanian,T. Billiar

Published 1998 in Journal of Biological Chemistry

ABSTRACT

It is now known that caspase-3-like protease activation can promote Bcl-2 cleavage and mitochondrial cytochromec release and that these events can lead to further downstream caspase activation. NO has been proposed as a potent, endogenous inhibitor of caspase-3-like protease activity. Experiments were carried out to determine whether NO could interrupt Bcl-2 cleavage or cytochrome c release by the inhibition of caspase activity linking these events. NO inhibited the capacity of purified caspase-3 to cleave recombinant Bcl-2. Both Bcl-2 cleavage and cytochrome c release were inhibited in tumor necrosis factor α- and actinomycin d-treated MCF-7 cells exposed to NO donors. The NO-mediated inhibition of Bcl-2 cleavage and cytochrome c release occurred in association with an inhibition of apoptosis and caspase-3-like activation. Thus, NO suppresses a key step in the positive feedback amplification of apoptotic signaling by preventing Bcl-2 cleavage and cytochromec release.

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