Document Detail


Signal transduction of nitric oxide donor-induced protection in hydrogen peroxide-mediated apoptosis in H9C2 cardiomyoblasts.
MedLine Citation:
PMID:  11417847     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
H J Chae; H R Kim; Y G Kwak; J K Ko; C U Joo; S W Chae
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Immunopharmacology and immunotoxicology     Volume:  23     ISSN:  0892-3973     ISO Abbreviation:  Immunopharmacol Immunotoxicol     Publication Date:  2001 May 
Date Detail:
Created Date:  2001-06-21     Completed Date:  2001-12-07     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  8800150     Medline TA:  Immunopharmacol Immunotoxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  187-204     Citation Subset:  IM    
Affiliation:
Institute of Cardiovascular Research, Chonkuk National University Medical School, Chonju, South Korea.
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MeSH Terms
Descriptor/Qualifier:
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:
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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