| Presentation of nitric oxide regulates monocyte survival through effects on caspase-9 and caspase-3 activation. | |
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MedLine Citation:
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PMID: 12566444 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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In the absence of survival factors, blood monocytes undergo spontaneous apoptosis, which involves the activation of caspase-3. Although nitric oxide can block caspase-3 activation and promote cell survival, it can also induce apoptosis. We hypothesized that nitrosothiols that promote protein S-nitrosylation would reduce caspase-3 activation and cell survival, whereas nitric oxide donors (such as 1-propamine 3-(2-hydroxy-2-nitroso-1-propylhydrazine (PAPA) NONOate and diethylamine (DEA) NONOate) that do not target thiol residues would not. Using human monocytes as a model, we observed that nitrosothiol donors S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine suppressed caspase-9 and caspase-3 activity and DNA fragmentation. In contrast, PAPA or DEA NONOate did not promote monocyte survival events and appeared to inhibit monocyte survival induced by macrophage colony-stimulating factor. The caspase-3-selective inhibitor DEVD-fluoromethyl ketone reversed DNA fragmentation events, and the caspase-9 inhibitor LEHD-fluoromethyl ketone reversed caspase-3 activity in monocytes treated with PAPA or DEA NONOate in the presence of macrophage colony-stimulating factor. These results were not caused by differences in glutathione levels or the kinetics of nitric oxide release. Moreover, S-nitrosoglutathione and S-nitroso-N-acetylpenicillamine directly blocked the activity of recombinant caspase-3, which was reversed by the reducing agent dithiothreitol, whereas PAPA or DEA NONOate did not block the enzymatic activity of caspase-3. These data support the hypothesis that nitrosylation of protein thiol residues by nitric oxide is critical for promoting the survival of human monocytes. |
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Authors:
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Mandy M Zeigler; Andrea I Doseff; Michelle F Galloway; Judy M Opalek; Philip T Nowicki; Jay L Zweier; Chandan K Sen; Clay B Marsh |
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Publication Detail:
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Type: In Vitro; Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2003-02-03 |
Journal Detail:
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Title: The Journal of biological chemistry Volume: 278 ISSN: 0021-9258 ISO Abbreviation: J. Biol. Chem. Publication Date: 2003 Apr |
Date Detail:
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Created Date: 2003-04-07 Completed Date: 2003-07-03 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 2985121R Medline TA: J Biol Chem Country: United States |
Other Details:
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Languages: eng Pagination: 12894-902 Citation Subset: IM |
Affiliation:
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Dorothy M. Davis Heart and Lung Research Institute, the Department of Internal Medicine, Ohio State University, Columbus, Ohio 43210-1252, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Caspase 3 Caspase 9 Caspases / blood* Cell Survival / drug effects* DNA Fragmentation / drug effects Enzyme Activation Glutathione / blood Humans Hydrazines / pharmacology Kinetics Monocytes / cytology*, drug effects, enzymology Nitric Oxide / pharmacology* Nitric Oxide Donors / pharmacology* Nitrogen Oxides S-Nitrosoglutathione |
| Grant Support | |
ID/Acronym/Agency:
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HL63800/HL/NHLBI NIH HHS; HL66108/HL/NHLBI NIH HHS; HL67176/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Hydrazines; 0/Nitric Oxide Donors; 0/Nitrogen Oxides; 0/PAPA NONOate; 10102-43-9/Nitric Oxide; 57564-91-7/S-Nitrosoglutathione; 70-18-8/Glutathione; 86831-65-4/1,1-diethyl-2-hydroxy-2-nitrosohydrazine; EC 3.4.22.-/CASP3 protein, human; EC 3.4.22.-/CASP9 protein, human; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspase 9; EC 3.4.22.-/Caspases |
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