{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,14]],"date-time":"2026-07-14T17:53:56Z","timestamp":1784051636848,"version":"3.55.0"},"reference-count":43,"publisher":"Oxford University Press (OUP)","issue":"14","license":[{"start":{"date-parts":[[2019,4,5]],"date-time":"2019-04-05T00:00:00Z","timestamp":1554422400000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"name":"DFG Excellence Cluster"},{"DOI":"10.13039\/100010447","name":"German Center for Cardiovascular Research","doi-asserted-by":"crossref","id":[{"id":"10.13039\/100010447","id-type":"DOI","asserted-by":"crossref"}]},{"name":"Cardio-Pulmonary Institute","award":["390649896"],"award-info":[{"award-number":["390649896"]}]},{"DOI":"10.13039\/501100001659","name":"Deutsche Forschungsgemeinschaft","doi-asserted-by":"publisher","award":["SFB 815\/Z1"],"award-info":[{"award-number":["SFB 815\/Z1"]}],"id":[{"id":"10.13039\/501100001659","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2019,12,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Aims<\/jats:title>\n                  <jats:p>The protein Scrib (Scribble 1) is known to control apico-basal polarity in epithelial cells. The role of polarity proteins in the vascular system remains poorly characterized; however, we previously reported that Scrib maintains the endothelial phenotype and directed migration. On this basis, we hypothesized that Scrib has anti-atherosclerotic functions.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods and results<\/jats:title>\n                  <jats:p>Tamoxifen-induced Scrib-knockout mice were crossed with ApoE\u2212\/\u2212 knockout mice and spontaneous atherosclerosis under high-fat diet (HFD), as well as accelerated atherosclerosis in response to partial carotid artery ligation and HFD, was induced. Deletion of Scrib resulted in increased atherosclerosis development in both models. Mechanistically, flow- as well as acetylcholine-induced endothelium-dependent relaxation and AKT phosphorylation was reduced by deletion of Scrib, whereas vascular permeability and leucocyte extravasation were increased after Scrib knockout. Scrib immune pull down in primary carotid endothelial cells and mass spectrometry identified Arhgef7 (Rho Guanine Nucleotide Exchange Factor 7, \u03b2Pix) as interaction partner. Scrib or Arhgef7 down-regulation by siRNA reduced the endothelial barrier function in human umbilical vein endothelial cells. Gene expression analysis from murine samples and from human biobank material of carotid endarterectomies indicated that loss of Scrib resulted in endothelial dedifferentiation with a decreased expression of endothelial signature genes.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusions<\/jats:title>\n                  <jats:p>By maintaining a quiescent endothelial phenotype, the polarity protein Scrib elicits anti-atherosclerotic functions.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/cvr\/cvz093","type":"journal-article","created":{"date-parts":[[2019,4,2]],"date-time":"2019-04-02T15:24:41Z","timestamp":1554218681000},"page":"1963-1974","source":"Crossref","is-referenced-by-count":14,"title":["The polarity protein Scrib limits atherosclerosis development in mice"],"prefix":"10.1093","volume":"115","author":[{"given":"Christoph","family":"Sch\u00fcrmann","sequence":"first","affiliation":[{"name":"Institute for 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Sluis","sequence":"additional","affiliation":[{"name":"Department of Pediatrics, Molecular Genetics Section, University of Groningen, University Medical Center Groningen, Antonius Deusinglaan 1, AV Groningen, The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Matthias S","family":"Leisegang","sequence":"additional","affiliation":[{"name":"Institute for Cardiovascular Physiology, Goethe-University, Theodor-Stern Kai 7, Frankfurt, Frankfurt am Main, Germany"},{"name":"German Center for Cardiovascular Research (DZHK), Partner Site RheinMain, Theodor-Stern Kai 7, Frankfurt, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stefan","family":"G\u00fcnther","sequence":"additional","affiliation":[{"name":"ECCPS Bioinformatics and Sequencing Facility, Goethe-University, Ludwigstrasse 43, Bad Nauheim, 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