High stretch induces endothelial dysfunction accompanied by oxidative stress and actin remodeling in human saphenous vein endothelial cells

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dc.contributorSistema FMUSP-HC: Faculdade de Medicina da Universidade de São Paulo (FMUSP) e Hospital das Clínicas da FMUSP
dc.contributor.authorGIRAO-SILVA, T.
dc.contributor.authorFONSECA-ALANIZ, M. H.
dc.contributor.authorRIBEIRO-SILVA, J. C.
dc.contributor.authorLEE, J.
dc.contributor.authorPATIL, N. P.
dc.contributor.authorDALLAN, L. A.
dc.contributor.authorBAKER, A. B.
dc.contributor.authorHARMSEN, M. C.
dc.contributor.authorKRIEGER, J. E.
dc.contributor.authorMIYAKAWA, A. A.
dc.date.accessioned2021-08-13T15:12:28Z
dc.date.available2021-08-13T15:12:28Z
dc.date.issued2021
dc.description.abstractThe rate of the remodeling of the arterialized saphenous vein conduit limits the outcomes of coronary artery bypass graft surgery (CABG), which may be influenced by endothelial dysfunction. We tested the hypothesis that high stretch (HS) induces human saphenous vein endothelial cell (hSVEC) dysfunction and examined candidate underlying mechanisms. Our results showed that in vitro HS reduces NO bioavailability, increases inflammatory adhesion molecule expression (E-selectin and VCAM1) and THP-1 cell adhesion. HS decreases F-actin in hSVECs, but not in human arterial endothelial cells, and is accompanied by G-actin and cofilin's nuclear shuttling and increased reactive oxidative species (ROS). Pre-treatment with the broad-acting antioxidant N-acetylcysteine (NAC) supported this observation and diminished stretch-induced actin remodeling and inflammatory adhesive molecule expression. Altogether, we provide evidence that increased oxidative stress and actin cytoskeleton remodeling play a role in HS-induced saphenous vein endothelial cell dysfunction, which may contribute to predisposing saphenous vein graft to failure.eng
dc.description.indexMEDLINEeng
dc.description.sponsorshipSao Paulo Research FoundationFundacao de Amparo a Pesquisa do Estado de Sao Paulo (FAPESP) [FAPESP 2013/17368-0]
dc.description.sponsorshipCoordination for the Improvement of Higher Education PersonnelCoordenacao de Aperfeicoamento de Pessoal de Nivel Superior (CAPES) [CAPES 88887.464006/2019-00]
dc.description.sponsorshipScience Without Borders (Ciencias sem Fronteiras) Program, Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [CNPq-401749/2012-6]
dc.description.sponsorshipAmerican Heart AssociationAmerican Heart Association [17IRG33410888]
dc.description.sponsorshipDOD CDMRPUnited States Department of Defense [W81XWH-16-1-0580, W81XWH-16-1-0582]
dc.description.sponsorshipNational Institutes of HealthUnited States Department of Health & Human ServicesNational Institutes of Health (NIH) - USA [1R21EB02355101, 1R21EB024147-01A1, 1R01HL141761-01]
dc.identifier.citationSCIENTIFIC REPORTS, v.11, n.1, article ID 13493, 14p, 2021
dc.identifier.doi10.1038/s41598-021-93081-3
dc.identifier.issn2045-2322
dc.identifier.urihttps://observatorio.fm.usp.br/handle/OPI/41325
dc.language.isoeng
dc.publisherNATURE RESEARCHeng
dc.relation.ispartofScientific Reports
dc.rightsopenAccesseng
dc.rights.holderCopyright NATURE RESEARCHeng
dc.subject.otherto-mesenchymal transitioneng
dc.subject.othernitric-oxideeng
dc.subject.otherintimal hyperplasiaeng
dc.subject.othermechanical stretcheng
dc.subject.othergraft failureeng
dc.subject.othercyclic straineng
dc.subject.otherresponseseng
dc.subject.otherphosphorylationeng
dc.subject.otherexpressioneng
dc.subject.othermechanotransductioneng
dc.subject.wosMultidisciplinary Scienceseng
dc.titleHigh stretch induces endothelial dysfunction accompanied by oxidative stress and actin remodeling in human saphenous vein endothelial cellseng
dc.typearticleeng
dc.type.categoryoriginal articleeng
dc.type.versionpublishedVersioneng
dspace.entity.typePublication
hcfmusp.affiliation.countryEstados Unidos
hcfmusp.affiliation.countryHolanda
hcfmusp.affiliation.countryisous
hcfmusp.affiliation.countryisonl
hcfmusp.author.externalLEE, J.:Univ Texas Austin, Dept Biomed Engn, Inst Cellular & Mol Biol, Inst Biomat Drug Delivery & Regenerat Med,Inst Co, Austin, TX USA
hcfmusp.author.externalPATIL, N. P.:Univ Texas Austin, Dept Biomed Engn, Inst Cellular & Mol Biol, Inst Biomat Drug Delivery & Regenerat Med,Inst Co, Austin, TX USA
hcfmusp.author.externalBAKER, A. B.:Univ Texas Austin, Dept Biomed Engn, Inst Cellular & Mol Biol, Inst Biomat Drug Delivery & Regenerat Med,Inst Co, Austin, TX USA
hcfmusp.author.externalHARMSEN, M. C.:Univ Groningen, Univ Med Ctr Groningen, Lab Cardiovasc Regenerat Med Res Grp CAVAREM, Dept Pathol & Med Biol, Groningen, Netherlands
hcfmusp.citation.scopus16
hcfmusp.contributor.author-fmusphcTHAIS GIRAO DA SILVA
hcfmusp.contributor.author-fmusphcMIRIAM HELENA FONSECA ALANIZ
hcfmusp.contributor.author-fmusphcJOAO CARLOS RIBEIRO DA SILVA
hcfmusp.contributor.author-fmusphcLUIS ALBERTO OLIVEIRA DALLAN
hcfmusp.contributor.author-fmusphcJOSE EDUARDO KRIEGER
hcfmusp.contributor.author-fmusphcAYUMI AUREA MIYAKAWA YAMAGUCHI
hcfmusp.description.articlenumber13493
hcfmusp.description.issue1
hcfmusp.description.volume11
hcfmusp.origemWOS
hcfmusp.origem.pubmed34188159
hcfmusp.origem.scopus2-s2.0-85109020044
hcfmusp.origem.wosWOS:000671782600006
hcfmusp.publisher.cityBERLINeng
hcfmusp.publisher.countryGERMANYeng
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