| Signal transduction of nitric oxide donor-induced protection in hydrogen peroxide-mediated apoptosis in H9C2 cardiomyoblasts. | |
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MedLine Citation:
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PMID: 11417847 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Nitric oxide (NO) attenuates hydrogen peroxide (H2O2)-mediated injury to H9C2 cardiomyoblasts. To examine the role of nitric oxide, cultured H9C2 cardiomyoblasts were treated with H2O2 for 2 h in the presence or absence of the NO donor, diethylamine nitric oxide (DEANO). DEANO (30 microM) attenuated H2O2-induced apoptosis in H9C2 cells. H2O2-exposed H9C2 cells resulted in apoptosis in a time-dependent manner estimated by DNA fragmentation assay, nuclear morphology stained with fluorescent dye, Hoechst 33258 and Annexin V staining. Pretreatment with z-VAD-FMK, a pancaspase inhibitor, or z-DEVD-CHO, a specific caspase-3 inhibitor, completely suppressed the DNA ladder in response to H2O2. An increase in caspase-3-like protease (DEVDase) activity was observed during apoptosis, but no caspase-1 activity (YVADase) was detected. Treatment of H9C2 cells with 100 microM H2O2, resulted in a strong activation of JNK/SAPK. However, the activation of JNK/ SAPK was clearly attenuated by 30 microM DEANO. Furthermore, the dominant negative JNK and SEK1-expressing cells displayed a marked decrease in a number of apoptotic cells. This inhibition of JNK1 in the system is involved in the protection of H2O2-induced apoptosis in H9C2 cardiomyoblasts. |
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Authors:
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H J Chae; H R Kim; Y G Kwak; J K Ko; C U Joo; S W Chae |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Immunopharmacology and immunotoxicology Volume: 23 ISSN: 0892-3973 ISO Abbreviation: Immunopharmacol Immunotoxicol Publication Date: 2001 May |
Date Detail:
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Created Date: 2001-06-21 Completed Date: 2001-12-07 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 8800150 Medline TA: Immunopharmacol Immunotoxicol Country: United States |
Other Details:
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Languages: eng Pagination: 187-204 Citation Subset: IM |
Affiliation:
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Institute of Cardiovascular Research, Chonkuk National University Medical School, Chonju, South Korea. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects*, physiology* Caspase 3 Caspases / metabolism Cell Line Cyclic GMP / metabolism Diethylamines / pharmacology Enzyme Activation / drug effects Heart / drug effects Hydrogen Peroxide / metabolism*, pharmacology JNK Mitogen-Activated Protein Kinases Mitogen-Activated Protein Kinases / metabolism Myocardium / cytology, metabolism Nitric Oxide Donors / pharmacology* Nitrogen Oxides Rats Reactive Oxygen Species / metabolism Signal Transduction |
| Chemical | |
Reg. No./Substance:
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0/Diethylamines; 0/Nitric Oxide Donors; 0/Nitrogen Oxides; 0/Reactive Oxygen Species; 7665-99-8/Cyclic GMP; 7722-84-1/Hydrogen Peroxide; 92818-79-6/diethylamine dinitric oxide adduct; EC 2.7.11.24/JNK Mitogen-Activated Protein Kinases; EC 2.7.11.24/Mitogen-Activated Protein Kinases; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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