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Increased Capillary Permeability in Heart Induces Diastolic Dysfunction Independently of Inflammation, Fibrosis, or Cardiomyocyte Dysfunction.

dc.rights.licenseopenen_US
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorABELANET, Alice
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCAMOIN, Marion
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorRUBIN, Sebastien
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorBOUGARAN, Pauline
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDELOBEL, Valentin
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorPERNOT, Mathieu
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorFORFAR, Isabelle
IDREF: 141977639
hal.structure.identifierInstitut des Maladies Métaboliques et Casdiovasculaires [UPS/Inserm U1297 - I2MC]
dc.contributor.authorGUILBEAU-FRUGIER, Céline
hal.structure.identifierInstitut des Maladies Métaboliques et Casdiovasculaires [UPS/Inserm U1297 - I2MC]
dc.contributor.authorGALÈS, Céline
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorBATS, Marie Lise
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorRENAULT, Marie-Ange
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDUFOURCQ, Pascale
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.authorDUPLÀA, Cécile
dc.date.accessioned2022-05-13T09:36:49Z
dc.date.available2022-05-13T09:36:49Z
dc.date.issued2022-05-05
dc.identifier.issn1524-4636en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/140051
dc.description.abstractEnWhile endothelial dysfunction is suggested to contribute to heart failure with preserved ejection fraction pathophysiology, understanding the importance of the endothelium alone, in the pathogenesis of diastolic abnormalities has not yet been fully elucidated. Here, we investigated the consequences of specific endothelial dysfunction on cardiac function, independently of any comorbidity or risk factor (diabetes or obesity) and their potential effect on cardiomyocyte. The ubiquitine ligase , expressed in endothelial cells (ECs), was shown to destabilize tight junction. A genetic mouse model in which is overexpressed in EC (iEC-Pdzrn3) in adults was developed. EC-specific expression increased cardiac leakage of IgG and fibrinogen blood-born molecules. The induced edema demonstrated features of diastolic dysfunction, with increased end-diastolic pressure, alteration of dP/dt min, increased natriuretic peptides, in addition to limited exercise capacity, without major signs of cardiac fibrosis and inflammation. Electron microscopic images showed edema with disrupted EC-cardiomyocyte interactions. RNA sequencing analysis of gene expression in cardiac EC demonstrated a decrease in genes coding for endothelial extracellular matrix proteins, which could be related to the fragile blood vessel phenotype. Irregularly shaped capillaries with hemorrhages were found in heart sections of iEC- mice. We also found that a high-fat diet was not sufficient to provoke diastolic dysfunction; high-fat diet aggravated cardiac inflammation, associated with an altered cardiac metabolic signature in EC- mice, reminiscent of heart failure with preserved ejection fraction features. An increase of endothelial permeability is responsible for mediating diastolic dysfunction pathophysiology and for aggravating detrimental effects of a high-fat diet on cardiac inflammation and metabolism.
dc.language.isoENen_US
dc.subjectARTICLE RECHERCHE
dc.title.enIncreased Capillary Permeability in Heart Induces Diastolic Dysfunction Independently of Inflammation, Fibrosis, or Cardiomyocyte Dysfunction.
dc.title.alternativeArterioscler Thromb Vasc Biolen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1161/ATVBAHA.121.317319en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
dc.identifier.pubmed35510550en_US
bordeaux.journalArteriosclerosis, Thrombosis, and Vascular Biologyen_US
bordeaux.page101161ATVBAHA121317319en_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.sourcepubmed
hal.identifierhal-03667268
hal.version1
hal.date.transferred2022-05-13T09:36:52Z
hal.exporttrue
workflow.import.sourcepubmed
dc.rights.ccPas de Licence CCen_US
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Arteriosclerosis,%20Thrombosis,%20and%20Vascular%20Biology&rft.date=2022-05-05&rft.spage=101161ATVBAHA121317319&rft.epage=101161ATVBAHA121317319&rft.eissn=1524-4636&rft.issn=1524-4636&rft.au=ABELANET,%20Alice&CAMOIN,%20Marion&RUBIN,%20Sebastien&BOUGARAN,%20Pauline&DELOBEL,%20Valentin&rft.genre=article


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