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Article: Senescence of cultured porcine coronary arterial endothelial cells is associated with accelerated oxidative stress and activation of nfκB

TitleSenescence of cultured porcine coronary arterial endothelial cells is associated with accelerated oxidative stress and activation of nfκB
Authors
Issue Date2010
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
Citation
Journal Of Vascular Research, 2010, v. 47 n. 4, p. 287-298 How to Cite?
AbstractAims: Endothelial dysfunction occurs following multiple passaging in vitro,but the molecular mechanisms involved remain unidentified. The present study defined the genomic changes related to dysfunction in cultured senescent endothelial cells. Methods and Results: Senescent cells were produced by multiple passaging of porcine coronary arterial endothelial cells for up to 4 weeks. Genomic and proteomic studies on cultured cells at the first passage (P1) and the fourth passage (P4) were performed. Senescence and decreased NO production were observed in cells and several signaling pathways-such as IFN/STAT, IGF, TGF-β, cytoskeleton rearrangement and lipid metabolism-were altered at P4, as judged from the microarray analysis. The basal and stimulated (by TNF-α) levels of NFκB were augmented in senescent cells in electrophoretic mobility shift assays in association with increased oxidative stress, increased p53 protein stability, and activated apoptotic pathways. The increased oxidative stress was alleviated by treatment with the superoxide dismutase mimetic MnTMPyP. Conclusions: After multiple passaging in vitro, porcine coronary endothelial cells exhibited dysfunction and senescence associated with reduced proliferative capacity, increased oxidative stress, and activation of the NFκB and p53 signaling pathways. © 2009 S. Karger AG, Basel.
Persistent Identifierhttp://hdl.handle.net/10722/171390
ISSN
2014 Impact Factor: 2.901
2014 SCImago Journal Rankings: 1.097
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorLee, MYKen_US
dc.contributor.authorWang, Yen_US
dc.contributor.authorVanhoutte, PMen_US
dc.date.accessioned2012-10-30T06:13:49Z-
dc.date.available2012-10-30T06:13:49Z-
dc.date.issued2010en_US
dc.identifier.citationJournal Of Vascular Research, 2010, v. 47 n. 4, p. 287-298en_US
dc.identifier.issn1018-1172en_US
dc.identifier.urihttp://hdl.handle.net/10722/171390-
dc.description.abstractAims: Endothelial dysfunction occurs following multiple passaging in vitro,but the molecular mechanisms involved remain unidentified. The present study defined the genomic changes related to dysfunction in cultured senescent endothelial cells. Methods and Results: Senescent cells were produced by multiple passaging of porcine coronary arterial endothelial cells for up to 4 weeks. Genomic and proteomic studies on cultured cells at the first passage (P1) and the fourth passage (P4) were performed. Senescence and decreased NO production were observed in cells and several signaling pathways-such as IFN/STAT, IGF, TGF-β, cytoskeleton rearrangement and lipid metabolism-were altered at P4, as judged from the microarray analysis. The basal and stimulated (by TNF-α) levels of NFκB were augmented in senescent cells in electrophoretic mobility shift assays in association with increased oxidative stress, increased p53 protein stability, and activated apoptotic pathways. The increased oxidative stress was alleviated by treatment with the superoxide dismutase mimetic MnTMPyP. Conclusions: After multiple passaging in vitro, porcine coronary endothelial cells exhibited dysfunction and senescence associated with reduced proliferative capacity, increased oxidative stress, and activation of the NFκB and p53 signaling pathways. © 2009 S. Karger AG, Basel.en_US
dc.languageengen_US
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVRen_US
dc.relation.ispartofJournal of Vascular Researchen_US
dc.subject.meshAnimalsen_US
dc.subject.meshAntioxidants - Pharmacologyen_US
dc.subject.meshCell Aging - Drug Effects - Geneticsen_US
dc.subject.meshCell Proliferation - Drug Effectsen_US
dc.subject.meshCells, Cultureden_US
dc.subject.meshCoronary Vessels - Drug Effects - Metabolismen_US
dc.subject.meshElectrophoretic Mobility Shift Assayen_US
dc.subject.meshEndothelial Cells - Drug Effects - Metabolismen_US
dc.subject.meshFemaleen_US
dc.subject.meshGene Expression Profiling - Methodsen_US
dc.subject.meshGene Expression Regulationen_US
dc.subject.meshMetalloporphyrins - Pharmacologyen_US
dc.subject.meshNf-Kappa B - Metabolismen_US
dc.subject.meshNitric Oxide - Metabolismen_US
dc.subject.meshOligonucleotide Array Sequence Analysisen_US
dc.subject.meshOxidative Stress - Drug Effects - Geneticsen_US
dc.subject.meshSignal Transductionen_US
dc.subject.meshSus Scrofaen_US
dc.subject.meshTime Factorsen_US
dc.subject.meshTumor Necrosis Factor-Alpha - Metabolismen_US
dc.subject.meshTumor Suppressor Protein P53 - Metabolismen_US
dc.titleSenescence of cultured porcine coronary arterial endothelial cells is associated with accelerated oxidative stress and activation of nfκBen_US
dc.typeArticleen_US
dc.identifier.emailWang, Y:yuwanghk@hku.hken_US
dc.identifier.emailVanhoutte, PM:vanhoutt@hku.hken_US
dc.identifier.authorityWang, Y=rp00239en_US
dc.identifier.authorityVanhoutte, PM=rp00238en_US
dc.description.naturelink_to_OA_fulltexten_US
dc.identifier.doi10.1159/000265563en_US
dc.identifier.pmid20016203en_US
dc.identifier.scopuseid_2-s2.0-72049129981en_US
dc.identifier.hkuros170961-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-72049129981&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume47en_US
dc.identifier.issue4en_US
dc.identifier.spage287en_US
dc.identifier.epage298en_US
dc.identifier.isiWOS:000278965000002-
dc.publisher.placeSwitzerlanden_US
dc.identifier.scopusauthoridLee, MYK=22980015700en_US
dc.identifier.scopusauthoridWang, Y=34973733700en_US
dc.identifier.scopusauthoridVanhoutte, PM=7202304247en_US
dc.identifier.citeulike10032812-

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