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.
Original language | English |
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Pages (from-to) | 2263-2269 |
Number of pages | 7 |
Journal | FEBS Letters |
Volume | 582 |
Issue number | 15 |
DOIs | |
State | Published - 25 Jun 2008 |
Externally published | Yes |
Keywords
- Apoptosis
- Ceramide 1-phosphate
- NF-κB
- Nitric oxide
- PI3-kinase
- Sphingolipids
ASJC Scopus subject areas
- Biophysics
- Structural Biology
- Biochemistry
- Molecular Biology
- Genetics
- Cell Biology