Abstract:
:Macrophages play vital roles in inflammatory responses, and their number at sites of inflammation is strictly regulated by cell death and division. Here, we demonstrate that production of nitric oxide (NO) is a major mechanism whereby ceramide-1-phosphate (C1P) blocks apoptosis in macrophages. However, NO failed to stimulate macrophage proliferation. The prosurvival effect of C1P was blocked by inhibitors of inducible NO synthase. The antiapoptotic effect of C1P was also blocked by phosphatidylinositol 3-kinase or nuclear factor-kappa B inhibitors. Moreover, NO reversed the inhibitory effect of C1P on acid sphingomyelinase, but the prosurvival effect of C1P was independent of this action.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Gangoiti P,Granado MH,Arana L,Ouro A,Gómez-Muñoz Adoi
10.1016/j.febslet.2008.05.027subject
Has Abstractpub_date
2008-06-25 00:00:00pages
2263-9issue
15eissn
0014-5793issn
1873-3468pii
S0014-5793(08)00439-0journal_volume
582pub_type
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