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PHACTR-1 (Phosphatase and Actin Regulator 1) Deficiency in Either Endothelial or Smooth Muscle Cells Does Not Predispose Mice to Nonatherosclerotic Arteriopathies in 3 Transgenic Mice.

dc.rights.licenseopenen_US
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.authorMARTIN, Soizic
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.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.authorJEANNINGROS, Sylvie
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorBATS, Marie-Lise
hal.structure.identifierBioingénierie tissulaire [BIOTIS]
dc.contributor.authorCOMBE, Christian
ORCID: 0000-0002-0360-573X
IDREF: 58708871
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDUFOURCQ, Pascale
hal.structure.identifierBordeaux population health [BPH]
dc.contributor.authorDEBETTE, Stephanie
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.accessioned2022-05-13T10:32:08Z
dc.date.available2022-05-13T10:32:08Z
dc.date.issued2022-05-01
dc.identifier.issn1524-4636en_US
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/140054
dc.description.abstractEnGenome-wide association studies have revealed robust associations of common genetic polymorphisms in an intron of the PHACTR-1 (phosphatase and actin regulator 1) gene (chr6p24), with cervical artery dissection, spontaneous coronary artery dissection, and fibromuscular dysplasia. The aim was to assess its role in the pathogenesis of cervical artery dissection or fibromuscular dysplasia. Using various tissue-specific Cre-driver mouse lines, was deleted either in endothelial cells using 2 tissue-specific Cre-driver (PDGFB [platelet-derived growth factor B]-Cre mice and Tie2 [tyrosine kinase with immunoglobulin and EGF homology domains]-Cre) and smooth muscle cells (smooth muscle actin-Cre) with a third tissue-specific Cre-driver. To test the efficacy of the deletion after cre-induction, we confirmed first, a decrease in Phactr1 transcription and Phactr1 expression in endothelial cell and smooth muscle cell isolated from Phactr1 and Phactr1 mice. Irrespective to the tissue or the duration of the deletion, mice did not spontaneously display pathological phenotype or vascular impairment: mouse survival, growth, blood pressure, large vessel morphology, or actin organization were not different in knockout mice than their comparatives littermates. Challenging vascular function and repair either by angiotensin II-induced hypertension or limb ischemia did not lead to vascular morphology or function impairment in Phactr1-deleted mice. Similarly, there were no more consequences of deletion during embryogenesis in endothelial cells. Loss of PHACTR-1 function in the cells involved in vascular physiology does not appear to induce a pathological vascular phenotype. The in vivo effect of the intronic variation described in genome-wide association studies is unlikely to involve downregulation in PHACTR-1 expression.
dc.language.isoENen_US
dc.subjectARTICLE RECHERCHE
dc.subject.enActins
dc.subject.enAnimals
dc.subject.enArterial Occlusive Diseases
dc.subject.enEndothelial Cells
dc.subject.enFibromuscular Dysplasia
dc.subject.enGenome-Wide Association Study
dc.subject.enMice
dc.subject.enKnockout
dc.subject.enTransgenic
dc.subject.enMicrofilament Proteins
dc.subject.enMyocytes
dc.subject.enSmooth Muscle
dc.subject.enPhosphoric Monoester Hydrolases
dc.title.enPHACTR-1 (Phosphatase and Actin Regulator 1) Deficiency in Either Endothelial or Smooth Muscle Cells Does Not Predispose Mice to Nonatherosclerotic Arteriopathies in 3 Transgenic Mice.
dc.title.alternativeArterioscler Thromb Vasc Biolen_US
dc.typeArticle de revueen_US
dc.identifier.doi10.1161/ATVBAHA.122.317431en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
dc.identifier.pubmed35387477en_US
bordeaux.journalArteriosclerosis, Thrombosis, and Vascular Biologyen_US
bordeaux.page597-609en_US
bordeaux.volume42en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires (BMC) - UMR 1034en_US
bordeaux.hal.laboratoriesBioingénierie Tissulaire (BioTis) - U1026
bordeaux.hal.laboratoriesBordeaux Population Health Research Center (BPH) - UMR 1219
bordeaux.issue5en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.institutionINSERMen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
bordeaux.import.sourcepubmed
hal.identifierhal-03667334
hal.version1
hal.date.transferred2022-05-13T10:32:10Z
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=2022-05-01&rft.volume=42&rft.issue=5&rft.spage=597-609&rft.epage=597-609&rft.eissn=1524-4636&rft.issn=1524-4636&rft.au=RUBIN,%20Sebastien&BOUGARAN,%20Pauline&MARTIN,%20Soizic&ABELANET,%20Alice&DELOBEL,%20Valentin&rft.genre=article


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