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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
2013 Impact Factor: 2.443
 
DOIhttp://dx.doi.org/10.1159/000265563
 
ISI Accession Number IDWOS:000278965000002
 
ReferencesReferences in Scopus
 
DC FieldValue
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.isiWOS:000278965000002
 
dc.identifier.issn1018-1172
2013 Impact Factor: 2.443
 
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
 
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<description.abstract>Aims: 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-&#946;, cytoskeleton rearrangement and lipid metabolism-were altered at P4, as judged from the microarray analysis. The basal and stimulated (by TNF-&#945;) levels of NF&#954;B 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 NF&#954;B and p53 signaling pathways. &#169; 2009 S. Karger AG, Basel.</description.abstract>
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Author Affiliations
  1. The University of Hong Kong Li Ka Shing Faculty of Medicine