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Anti-integrin α(v) therapy improves cardiac fibrosis after myocardial infarction by blunting cardiac PW1(+) stromal cells

dc.rights.licenseopenen_US
dc.contributor.authorBOUVET, M.
dc.contributor.authorCLAUDE, O.
dc.contributor.authorROUX, M.
dc.contributor.authorSKELLY, D.
dc.contributor.authorMASURKAR, N.
dc.contributor.authorMOUGENOT, N.
dc.contributor.authorNADAUD, S.
dc.contributor.authorBLANC, C.
dc.contributor.authorDELACROIX, C.
dc.contributor.authorCHARDONNET, S.
dc.contributor.authorPIONNEAU, C.
dc.contributor.authorPERRET, C.
dc.contributor.authorYANIZ-GALENDE, E.
dc.contributor.authorROSENTHAL, N.
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorTREGOUET, David-Alexandre
dc.contributor.authorMARAZZI, G.
dc.contributor.authorSILVESTRE, J. S.
dc.contributor.authorSASSOON, D.
dc.contributor.authorHULOT, J. S.
dc.date.accessioned2021-01-18T11:17:35Z
dc.date.available2021-01-18T11:17:35Z
dc.date.issued2020
dc.identifier.issn2045-2322en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/25815
dc.description.abstractEnThere is currently no therapy to limit the development of cardiac fibrosis and consequent heart failure. We have recently shown that cardiac fibrosis post-myocardial infarction (MI) can be regulated by resident cardiac cells with a fibrogenic signature and identified by the expression of PW1 (Peg3). Here we identify αV-integrin (CD51) as an essential regulator of cardiac PW1+ cells fibrogenic behavior. We used transcriptomic and proteomic approaches to identify specific cell-surface markers for cardiac PW1+ cells and found that αV-integrin (CD51) was expressed in almost all cardiac PW1+ cells (93% ± 1%), predominantly as the αVβ1 complex. αV-integrin is a subunit member of the integrin family of cell adhesion receptors and was found to activate complex of latent transforming growth factor beta (TGFβ at the surface of cardiac PW1+ cells. Pharmacological inhibition of αV-integrin reduced the profibrotic action of cardiac PW1+CD51+ cells and was associated with improved cardiac function and animal survival following MI coupled with a reduced infarct size and fibrotic lesion. These data identify a targetable pathway that regulates cardiac fibrosis in response to an ischemic injury and demonstrate that pharmacological inhibition of αV-integrin could reduce pathological outcomes following cardiac ischemia.
dc.language.isoENen_US
dc.rightsAttribution 3.0 United States*
dc.rights.urihttp://creativecommons.org/licenses/by/3.0/us/*
dc.subjectVINTAGE
dc.title.enAnti-integrin α(v) therapy improves cardiac fibrosis after myocardial infarction by blunting cardiac PW1(+) stromal cells
dc.title.alternativeSci Repen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1038/s41598-020-68223-8en_US
dc.subject.halSciences du Vivant [q-bio]/Santé publique et épidémiologieen_US
dc.identifier.pubmed32647159en_US
bordeaux.journalSci Repen_US
bordeaux.page11404en_US
bordeaux.volume10en_US
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - UMR 1219en_US
bordeaux.issue1en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.teamVINTAGEen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
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