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J Biol Chem, Vol. 274, Issue 11, 7190-7195, March 12, 1999
From the Exogenous NO is able to trigger
apoptosis of renal mesangial cells, and thus may contribute to
acute lytic phases as well as to resolution of glomerulonephritis.
However, the mechanism involved in these events is still unclear. We
report here that chronic exposure of renal mesangial cells for 24 h to compounds releasing NO, including spermine-NO,
(Z)-1-{N-methyl-N-[6-(N-methylammoniohexyl)amino]}diazen-1-ium-1,2-diolate (MAHMA-NO), S-nitrosoglutathione (GS-NO), and
S-nitroso-N-acetyl-D,L-penicillamine (SNAP) results in a potent and dose-dependent increase in
the lipid signaling molecule ceramide. Time courses reveal that
significant effects occur after 2-4 h of stimulation with NO donors
and reach maximal levels after 24 h of stimulation. No acute
(within minutes) ceramide production can be detected. When cells were
stimulated with NO donors in the presence of phorbol ester, a direct
activator of protein kinase C, both ceramide production and DNA
fragmentation are completely abolished. Furthermore, addition of
exogenous ceramide partially reversed the inhibitory effect of phorbol
ester on apoptosis, thus suggesting a negative regulation of protein
kinase C on ceramide formation and apoptosis. In contrast to exogenous
NO, tumor necrosis factor (TNF)- Interestingly, NO and TNF In summary, our data demonstrate that exogenous NO causes a chronic
up-regulation of ceramide levels in mesangial cells by activating
sphingomyelinases and concomitantly inhibiting ceramidases, and that
particularly the late-phase of ceramide generation may be responsible
for the further processing of a proapoptotic signal.
Nitric Oxide Donors Induce Stress Signaling via Ceramide
Formation in Rat Renal Mesangial Cells
§,
Center for Biomembranes and Lipid
Enzymology, University of Utrecht, Padualaan 8, 3584 CH Utrecht, The
Netherlands and § Zentrum der Pharmakologie, Klinikum der
Johann Wolfgang Goethe-Universität, D-60590 Frankfurt am Main,
Germany
stimulates a very rapid and
transient increase in ceramide levels within minutes but fails to
induce the late-phase ceramide formation. Moreover, TNF fails to
induce apoptosis in mesangial cells.
cause a chronic activation of acidic and
neutral sphingomyelinases, the ceramide-generating enzymes, whereas
acidic and neutral ceramidases, the ceramide-metabolizing enzymes, are
inhibited by NO, but potently stimulated by TNF. Furthermore, in the
presence of an acidic ceramidase inhibitor, N-oleoylethanolamine, TNF leads to a sustained
accumulation of ceramide and in parallel induces DNA fragmentation.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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