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Fzd7 (Frizzled-7) Expressed by Endothelial Cells Controls Blood Vessel Formation Through Wnt/β-Catenin Canonical Signaling.

dc.rights.licenseopenen_US
dc.contributor.authorPEGHAIRE, C.
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorBATS, M. L.
dc.contributor.authorSEWDUTH, R. N.
dc.contributor.authorJEANNINGROS, S.
dc.contributor.authorJASPARD, B.
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorCOUFFINHAL, T.
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDUPLAA-COUFFINHAL, Cécile
hal.structure.identifierBiologie des maladies cardiovasculaires = Biology of Cardiovascular Diseases
dc.contributor.authorDUFOURCQ, P.
dc.date.accessioned2020-10-28T12:26:35Z
dc.date.available2020-10-28T12:26:35Z
dc.date.issued2016-12
dc.identifier.urihttps://oskar-bordeaux.fr/handle/20.500.12278/11536
dc.description.abstractEnAbstract OBJECTIVE: Vessel formation requires precise orchestration of a series of morphometric and molecular events controlled by a multitude of angiogenic factors and morphogens. Wnt/frizzled signaling is required for proper vascular formation. In this study, we investigated the role of the Fzd7 (frizzled-7) receptor in retinal vascular development and its relationship with the Wnt/β-catenin canonical pathway and Notch signaling. APPROACH AND RESULTS: Using transgenic mice, we demonstrated that Fzd7 is required for postnatal vascular formation. Endothelial cell (EC) deletion of fzd7 (fzd7ECKO) delayed retinal plexus formation because of an impairment in tip cell phenotype and a decrease in stalk cell proliferation. Dvl (dishevelled) proteins are a main component of Wnt signaling and play a functionally redundant role. We found that Dvl3 depletion in dvl1-/- mice mimicked the fzd7ECKO vascular phenotype and demonstrated that Fzd7 acted via β-catenin activation by showing that LiCl treatment rescued impairment in tip and stalk cell phenotypes induced in fzd7 mutants. Deletion of fzd7 or Dvl1/3 induced a strong decrease in Wnt canonical genes and Notch partners' expression. Genetic and pharmacological rescue strategies demonstrated that Fzd7 acted via β-catenin activation, upstream of Notch signaling to control Dll4 and Jagged1 EC expression. CONCLUSIONS: Fzd7 expressed by EC drives postnatal angiogenesis via activation of Dvl/β-catenin signaling and can control the integrative interaction of Wnt and Notch signaling during postnatal angiogenesis.
dc.language.isoENen_US
dc.subject*Article RECHERCHE
dc.subject.enCardiovascular Diseases
dc.subject.enEndothelial Cells
dc.subject.enFrizzled Receptor
dc.subject.enNeovascularization
dc.subject.enTransgenic Mice
dc.title.enFzd7 (Frizzled-7) Expressed by Endothelial Cells Controls Blood Vessel Formation Through Wnt/β-Catenin Canonical Signaling.
dc.typeArticle de revueen_US
dc.identifier.doihttps://doi.org/10.1161/ATVBAHA.116.307926en_US
dc.subject.halSciences du Vivant [q-bio]/Médecine humaine et pathologieen_US
bordeaux.journalArteriosclerosis, Thrombosis, and Vascular Biologyen_US
bordeaux.page2369–2380en_US
bordeaux.volume36en_US
bordeaux.hal.laboratoriesBiologie des maladies cardiovasculaires - U1034en_US
bordeaux.issue12en_US
bordeaux.institutionUniversité de Bordeauxen_US
bordeaux.peerReviewedouien_US
bordeaux.inpressnonen_US
hal.exportfalse
bordeaux.COinSctx_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.jtitle=Arteriosclerosis,%20Thrombosis,%20and%20Vascular%20Biology&rft.date=2016-12&rft.volume=36&rft.issue=12&rft.spage=2369%E2%80%932380&rft.epage=2369%E2%80%932380&rft.au=PEGHAIRE,%20C.&BATS,%20M.%20L.&SEWDUTH,%20R.%20N.&JEANNINGROS,%20S.&JASPARD,%20B.&rft.genre=article


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