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

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TitleSenescence of cultured porcine coronary arterial endothelial cells is associated with accelerated oxidative stress and activation of nfκB
AuthorsLee, MYK1
Wang, Y1
Vanhoutte, PM1
Issue Date2010
PublisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
CitationJournal Of Vascular Research, 2010, v. 47 n. 4, p. 287-298 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000265563
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.
ISSN1018-1172
2011 Impact Factor: 2.651
2011 SCImago Journal Rankings: 0.218
DOIhttp://dx.doi.org/10.1159/000265563
ReferencesReferences in Scopus
DC Field
Value
dc.contributor.authorLee, MYK
dc.contributor.authorWang, Y
dc.contributor.authorVanhoutte, PM
dc.date.accessioned2012-10-30T06:13:49Z
dc.date.available2012-10-30T06:13:49Z
dc.date.issued2010
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.
dc.description.natureLink_to_subscribed_fulltext
dc.identifier.citationJournal Of Vascular Research, 2010, v. 47 n. 4, p. 287-298 [How to Cite?]
DOI: http://dx.doi.org/10.1159/000265563
dc.identifier.citeulike10032812
dc.identifier.doihttp://dx.doi.org/10.1159/000265563
dc.identifier.epage298
dc.identifier.issn1018-1172
2011 Impact Factor: 2.651
2011 SCImago Journal Rankings: 0.218
dc.identifier.issue4
dc.identifier.pmid20016203
dc.identifier.scopuseid_2-s2.0-72049129981
dc.identifier.spage287
dc.identifier.urihttp://hdl.handle.net/10722/171390
dc.identifier.volume47
dc.languageeng
dc.publisherS Karger AG. The Journal's web site is located at http://www.karger.com/JVR
dc.publisher.placeSwitzerland
dc.relation.ispartofJournal of Vascular Research
dc.relation.referencesReferences in Scopus
dc.subject.meshAnimals
dc.subject.meshAntioxidants - Pharmacology
dc.subject.meshCell Aging - Drug Effects - Genetics
dc.subject.meshCell Proliferation - Drug Effects
dc.subject.meshCells, Cultured
dc.subject.meshCoronary Vessels - Drug Effects - Metabolism
dc.subject.meshElectrophoretic Mobility Shift Assay
dc.subject.meshEndothelial Cells - Drug Effects - Metabolism
dc.subject.meshFemale
dc.subject.meshGene Expression Profiling - Methods
dc.subject.meshGene Expression Regulation
dc.subject.meshMetalloporphyrins - Pharmacology
dc.subject.meshNf-Kappa B - Metabolism
dc.subject.meshNitric Oxide - Metabolism
dc.subject.meshOligonucleotide Array Sequence Analysis
dc.subject.meshOxidative Stress - Drug Effects - Genetics
dc.subject.meshSignal Transduction
dc.subject.meshSus Scrofa
dc.subject.meshTime Factors
dc.subject.meshTumor Necrosis Factor-Alpha - Metabolism
dc.subject.meshTumor Suppressor Protein P53 - Metabolism
dc.titleSenescence of cultured porcine coronary arterial endothelial cells is associated with accelerated oxidative stress and activation of nfκB
dc.typeArticle
Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine