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Partial Mural Cell Ablation Disrupts Coronary Vasculature Integrity and Induces Systolic Dysfunction

dc.rights.licenseopenen_US
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCORNUAULT, Lauriane
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorHÉRION, François‐xavier
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorBOURGUIGNON, Célia
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorROUAULT, Paul
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorFOUSSARD, Ninon
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorALZIEU, Philippe
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCHAPOULY, Candice
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorGADEAU, Alain‐pierre
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCOUFFINHAL, Thierry
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorRENAULT, Marie‐ange
dc.date.accessioned2024-01-16T14:49:17Z
dc.date.available2024-01-16T14:49:17Z
dc.date.issued2023-06-22
dc.identifier.issn2047-9980en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/187275
dc.description.abstractEnBackground Although the critical role of pericytes in maintaining vascular integrity has been extensively demonstrated in the brain and the retina, little is known about their role in the heart. We aim to investigate structural and functional consequences of partial pericyte depletion (≈60%) in the heart of adult mice. Methods and Results To deplete pericytes in adult mice, we used platelet‐derived growth factor receptor β–Cre/ERT2; Rosa DTA mice and compared their phenotype with that of control mice (Rosa DTA ) chosen among their littermates. Cardiac function was assessed via echocardiography and left ventricular catheterization 1 month after the first tamoxifen injection. We found mice depleted with pericytes had a reduced left ventricular ejection fraction and an increased end‐diastolic pressure, demonstrating both systolic and diastolic dysfunction. Consistently, mice depleted with pericytes presented a decreased left ventricular contractility and an increased left ventricular relaxation time (dP/dt min ). At the tissue level, mice depleted of pericytes displayed increased coronary endothelium leakage and activation, which was associated with increased CD45 + cell infiltration. Consistent with systolic dysfunction, pericyte depletion was associated with an increased expression of myosin heavy chain 7 and decreased expression of ATPase sarcoplasmic/endoplasmic reticulum Ca2 + transporting 2 and connexin 43. More important, coculture assays demonstrated, for the first time, that the decreased expression of connexin 43 is likely attributable to a direct effect of pericytes on cardiomyocytes. Besides, this study reveals that cardiac pericytes may undergo strong remodeling on injury. Conclusions Cardiac pericyte depletion induces both systolic and diastolic dysfunction, suggesting that pericyte dysfunction may contribute to the occurrence of cardiac diseases.
dc.description.sponsorshipLa dysfonction endothéliale dans l'insuffisance cardiaque à fraction d'éjection préservée - ANR-19-CE14-0025en_US
dc.language.isoENen_US
dc.subject.enPericytes heart coronary micro-vasculature cardiac function
dc.subject.enPericytes
dc.subject.enheart
dc.subject.encoronary micro-vasculature
dc.subject.encardiac function
dc.title.enPartial Mural Cell Ablation Disrupts Coronary Vasculature Integrity and Induces Systolic Dysfunction
dc.typeArticle de revueen_US
dc.identifier.doi10.1161/JAHA.122.029279en_US
dc.subject.halSciences du Vivant [q-bio]en_US
bordeaux.journalJournal of the American Heart Associationen_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcehal
hal.identifierinserm-04139340
hal.version1
hal.popularnonen_US
hal.audienceInternationaleen_US
hal.exportfalse
workflow.import.sourcehal
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Journal%20of%20the%20American%20Heart%20Association&rft.date=2023-06-22&rft.eissn=2047-9980&rft.issn=2047-9980&rft.au=CORNUAULT,%20Lauriane&H%C3%89RION,%20Fran%C3%A7ois%E2%80%90xavier&BOURGUIGNON,%20C%C3%A9lia&ROUAULT,%20Paul&FOUSSARD,%20Ninon&rft.genre=article


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