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Article: Nitric oxide and oxygen radicals induced apoptosis via bcl-2 and p53 pathway in hypoxia-reoxygenated cardiomyocytes

TitleNitric oxide and oxygen radicals induced apoptosis via bcl-2 and p53 pathway in hypoxia-reoxygenated cardiomyocytes
Authors
Issue Date2003
Publisher中國科學院. The Journal's web site is located at http://jcxg.chinajournal.net.cn/
Citation
Science In China, Series C: Life Sciences, 2003, v. 46 n. 1, p. 28-39 How to Cite?
AbstractNeonatal rat cardiomyocytes were subjected to 24 h of hypoxia 95%N 2/5%CO2 and 24 h of hypoxia plus 4 h of reoxygenation 95%O2/5%CO2. 24 h of hypoxia increased the levels of NO, NO2 -/NO3 -, TBARS and LDH. 24 h of hypoxia plus 4 h of reoxygenation decreased the levels of NO, NO 2 -/NO3 -, but further increased TBARS and LDH. The hypoxia up-regulated the expression of bcl-2, p53 and p21/waf1/cip1 but the reoxygenation down-regulated the expression of bcl-2, and further up-regulated p53 and p21/waf1/cip1. The hypoxia increased cell apoptosis and reoxygenation further increased both apoptotic and necrotic cell death. NO, NO2/NO3 -, TBARS, DNA fragmentation and cell apoptosis were enhanced by SNP and inhibited by L-NAME respectively. In addition, SOD/catalase down-regulated the expression of p53, p21/waf1/cipl and TEARS but up-regulated bcl-2 and increased indirectly the level of NO, NO 2 -/NO3 -, and inhibited DNA fragmentation. The results suggest that hypoxia-induced cell death is associated with the activation of NO, bcl-2 and p53 pathway, while hypoxia-reoxygenation induced cell death via the generation of reactive oxygen species and activation of p53 pathway. The present study clarified that NO may be an initiative signal to apoptotic cell death and the activation of bcl-2, p53 and p21/waf1/cip1 pathway in hypoxic and hypoxia-reoxygenated cardiomyocytes.
Persistent Identifierhttp://hdl.handle.net/10722/77796
ISSN
2011 Impact Factor: 1.61
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorShen, Jen_HK
dc.contributor.authorQiu, Xen_HK
dc.contributor.authorJiang, Ben_HK
dc.contributor.authorZhang, Den_HK
dc.contributor.authorXin, Wen_HK
dc.contributor.authorFung, PCWen_HK
dc.contributor.authorZhao, Ben_HK
dc.date.accessioned2010-09-06T07:35:49Z-
dc.date.available2010-09-06T07:35:49Z-
dc.date.issued2003en_HK
dc.identifier.citationScience In China, Series C: Life Sciences, 2003, v. 46 n. 1, p. 28-39en_HK
dc.identifier.issn1006-9305en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77796-
dc.description.abstractNeonatal rat cardiomyocytes were subjected to 24 h of hypoxia 95%N 2/5%CO2 and 24 h of hypoxia plus 4 h of reoxygenation 95%O2/5%CO2. 24 h of hypoxia increased the levels of NO, NO2 -/NO3 -, TBARS and LDH. 24 h of hypoxia plus 4 h of reoxygenation decreased the levels of NO, NO 2 -/NO3 -, but further increased TBARS and LDH. The hypoxia up-regulated the expression of bcl-2, p53 and p21/waf1/cip1 but the reoxygenation down-regulated the expression of bcl-2, and further up-regulated p53 and p21/waf1/cip1. The hypoxia increased cell apoptosis and reoxygenation further increased both apoptotic and necrotic cell death. NO, NO2/NO3 -, TBARS, DNA fragmentation and cell apoptosis were enhanced by SNP and inhibited by L-NAME respectively. In addition, SOD/catalase down-regulated the expression of p53, p21/waf1/cipl and TEARS but up-regulated bcl-2 and increased indirectly the level of NO, NO 2 -/NO3 -, and inhibited DNA fragmentation. The results suggest that hypoxia-induced cell death is associated with the activation of NO, bcl-2 and p53 pathway, while hypoxia-reoxygenation induced cell death via the generation of reactive oxygen species and activation of p53 pathway. The present study clarified that NO may be an initiative signal to apoptotic cell death and the activation of bcl-2, p53 and p21/waf1/cip1 pathway in hypoxic and hypoxia-reoxygenated cardiomyocytes.en_HK
dc.languageengen_HK
dc.publisher中國科學院. The Journal's web site is located at http://jcxg.chinajournal.net.cn/en_HK
dc.relation.ispartofScience in China, Series C: Life Sciencesen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshApoptosis - drug effects - physiologyen_HK
dc.subject.meshCell Hypoxia - drug effects - physiologyen_HK
dc.subject.meshCyclin-Dependent Kinase Inhibitor p21 - metabolismen_HK
dc.subject.meshL-Lactate Dehydrogenase - metabolismen_HK
dc.subject.meshMyocytes, Cardiac - cytology - drug effects - metabolismen_HK
dc.subject.meshNG-Nitroarginine Methyl Ester - pharmacologyen_HK
dc.subject.meshNitric Oxide - metabolism - pharmacologyen_HK
dc.subject.meshNitroprusside - pharmacologyen_HK
dc.subject.meshProto-Oncogene Proteins c-bcl-2 - metabolismen_HK
dc.subject.meshRatsen_HK
dc.subject.meshReactive Oxygen Species - metabolism - pharmacologyen_HK
dc.subject.meshSignal Transductionen_HK
dc.subject.meshThiobarbituric Acid Reactive Substances - metabolismen_HK
dc.subject.meshTumor Suppressor Protein p53 - metabolismen_HK
dc.titleNitric oxide and oxygen radicals induced apoptosis via bcl-2 and p53 pathway in hypoxia-reoxygenated cardiomyocytesen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0036-8237&volume=46&issue=1&spage=28&epage=39&date=2003&atitle=Nitric+oxide+and+oxygen+radicals+induced+apoptosis+via+bcl-2+and+p53+pathway+in+hypoxia-reoxygenated+cardiomyocytes.en_HK
dc.identifier.emailShen, J: shenjg@hku.hken_HK
dc.identifier.authorityShen, J=rp00487en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1360/03yc9004en_HK
dc.identifier.pmid20213359-
dc.identifier.scopuseid_2-s2.0-33646761286en_HK
dc.identifier.hkuros83943en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-33646761286&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume46en_HK
dc.identifier.issue1en_HK
dc.identifier.spage28en_HK
dc.identifier.epage39en_HK
dc.identifier.isiWOS:000181332000004-
dc.publisher.placeChinaen_HK
dc.identifier.scopusauthoridShen, J=7404929947en_HK
dc.identifier.scopusauthoridQiu, X=36095502300en_HK
dc.identifier.scopusauthoridJiang, B=34770534200en_HK
dc.identifier.scopusauthoridZhang, D=8094319900en_HK
dc.identifier.scopusauthoridXin, W=7102977683en_HK
dc.identifier.scopusauthoridFung, PCW=7101613315en_HK
dc.identifier.scopusauthoridZhao, B=7403058931en_HK

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