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dc.rights.licenseopenen_US
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.authorBATS, Marie Lise
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.authorRUBIN, Sébastien
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorVAURS, Juliette
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.authorDUPLAA, Cecile
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDUFOURCQ, Pascale
dc.date.accessioned2023-11-03T17:15:59Z
dc.date.available2023-11-03T17:15:59Z
dc.date.issued2023-07-01
dc.identifier.issn1524-4636en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/184593
dc.description.abstractEnEndothelial cells (ECs) are sensitive to physical forces created by blood flow, especially to laminar shear stress. Among the cell responses to laminar flow, EC polarization against the flow direction emerges as a key event, particularly during the development and remodeling of the vascular network. EC adopt an elongated planar cell shape with an asymmetrical distribution of intracellular organelles along the axis of blood flow. This study aimed to investigate the involvement of planar cell polarity via the receptor ROR2 (receptor tyrosine kinase-like orphan receptor 2) in endothelial responses to laminar shear stress. We generated a genetic mouse model with EC-specific deletion of , in combination with in vitro approaches involving loss- and gain-of-function experiments. During the first 2 weeks of life, the endothelium of the mouse aorta undergoes a rapid remodeling associated with a loss of EC polarization against the flow direction. Notably, we found a correlation between ROR2 expression and endothelial polarization levels. Our findings demonstrate that deletion of in murine ECs impaired their polarization during the postnatal development of the aorta. In vitro experiments further validated the essential role of ROR2 in both EC collective polarization and directed migration under laminar flow conditions. Exposure to laminar shear stress triggered the relocalization of ROR2 to cell-cell junctions where it formed a complex with VE-Cadherin and β-catenin, thereby regulating adherens junctions remodeling at the rear and front poles of ECs. Finally, we showed that adherens junctions remodeling and cell polarity induced by ROR2 were dependent on the activation of the small GTPase Cdc42. This study identified ROR2/planar cell polarity pathway as a new mechanism controlling and coordinating collective polarity patterns of EC during shear stress response.
dc.language.isoENen_US
dc.subject.enMice
dc.subject.enAnimals
dc.subject.enEndothelial Cells
dc.subject.enReceptor Tyrosine Kinase-like Orphan Receptors
dc.subject.enCell Polarity
dc.subject.enEndothelium
dc.subject.enVascular
dc.subject.enIntercellular Junctions
dc.subject.enStress
dc.subject.enMechanical
dc.title.enROR2/PCP a New Pathway Controlling Endothelial Cell Polarity Under Flow Conditions.
dc.title.alternativeArterioscler Thromb Vasc Biolen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1161/ATVBAHA.123.319106en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
dc.identifier.pubmed37199159en_US
bordeaux.journalArteriosclerosis, Thrombosis, and Vascular Biologyen_US
bordeaux.page1199-1218en_US
bordeaux.volume43en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.issue7en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.identifierhal-04270103
hal.version1
hal.date.transferred2023-11-03T17:16:01Z
hal.popularnonen_US
hal.audienceInternationaleen_US
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=2023-07-01&rft.volume=43&rft.issue=7&rft.spage=1199-1218&rft.epage=1199-1218&rft.eissn=1524-4636&rft.issn=1524-4636&rft.au=BOUGARAN,%20Pauline&BATS,%20Marie%20Lise&DELOBEL,%20Valentin&RUBIN,%20S%C3%A9bastien&VAURS,%20Juliette&rft.genre=article


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