{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,22]],"date-time":"2026-10-22T23:02:04Z","timestamp":1792710124011,"version":"4.5.0"},"reference-count":52,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["ATVB"],"published-print":{"date-parts":[[2012,8]]},"abstract":"<jats:sec>\n            <jats:title>Objective\u2014<\/jats:title>\n            <jats:p>Deep vein thrombosis (DVT) and pulmonary embolism are frequent causes of morbidity and mortality. The goal of our study was to determine whether plasma high-density lipoprotein (HDL), which inversely correlates with the risk of cardiovascular events, affects DVT.<\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Methods and Results\u2014<\/jats:title>\n            <jats:p>\n              Using a murine DVT model of inferior vena cava stenosis, we demonstrated that deficiency of the HDL receptor, scavenger receptor class B type I (SR-BI), promotes venous thrombosis. As SR-BI\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice have increased plasma cholesterol levels and abnormal HDL particles, we tested SR-BI\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice with an SR-BI liver transgene that normalizes both parameters. These mice also exhibited increased susceptibility to DVT, indicating a protective role of extrahepatic SR-BI. Mice lacking the major HDL apolipoprotein apoA-I or endothelial nitric oxide synthase (eNOS) (a downstream target of endothelial SR-BI signaling) also had a prothrombotic phenotype. Intravenous infusion of human apoA-I, an HDL component and SR-BI ligend, prevented DVT in wild-type but not SR-BI\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              or eNOS\n              <jats:sup>\u2212\/\u2212<\/jats:sup>\n              mice, suggesting that its effect is mediated by SR-BI and eNOS. Intravenous apoA-I infusion abolished histamine-induced platelet\u2013endothelial interactions, which are important for DVT initiation.\n            <\/jats:p>\n          <\/jats:sec>\n          <jats:sec>\n            <jats:title>Conclusion\u2014<\/jats:title>\n            <jats:p>An apoA-I (HDL)\u2013SR-BI\u2013eNOS axis is highly protective in DVT and may provide new targets for prophylaxis and treatment of venous thrombosis.<\/jats:p>\n          <\/jats:sec>","DOI":"10.1161\/atvbaha.112.252130","type":"journal-article","created":{"date-parts":[[2012,6,1]],"date-time":"2012-06-01T04:47:46Z","timestamp":1338526066000},"page":"1841-1847","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":49,"title":["Extrahepatic High-Density Lipoprotein Receptor SR-BI and ApoA-I Protect Against Deep Vein Thrombosis in Mice"],"prefix":"10.1161","volume":"32","author":[{"given":"Alexander","family":"Brill","sequence":"first","affiliation":[{"name":"From the Immune Disease Institute (A.B., S.F.D.M., T.A.F., D.D.W.), Program in Cellular and Molecular Medicine, Children\u2019s Hospital Boston (A.B., S.F.D.M., T.A.F., D.D.W.), and Department of Pediatrics (A.B., S.F.D.M., T.A.F., D.D.W.), Harvard Medical School, Boston, MA; Biology Department, Massachusetts Institute of Technology, Cambridge, MA (A.Y., J.K., M.K.); Department of Pathology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA ..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ayce","family":"Yesilaltay","sequence":"additional","affiliation":[{"name":"From the Immune Disease Institute (A.B., S.F.D.M., T.A.F., D.D.W.), Program in Cellular and Molecular Medicine, Children\u2019s Hospital Boston (A.B., S.F.D.M., T.A.F., D.D.W.), and Department of Pediatrics (A.B., S.F.D.M., T.A.F., D.D.W.), Harvard Medical School, Boston, MA; Biology Department, Massachusetts Institute of Technology, Cambridge, MA (A.Y., J.K., M.K.); Department of Pathology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA ..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Simon F.","family":"De Meyer","sequence":"additional","affiliation":[{"name":"From the Immune Disease Institute (A.B., S.F.D.M., T.A.F., D.D.W.), Program in Cellular and Molecular Medicine, Children\u2019s Hospital Boston (A.B., S.F.D.M., T.A.F., D.D.W.), and Department of Pediatrics (A.B., S.F.D.M., T.A.F., D.D.W.), Harvard Medical School, Boston, MA; Biology Department, Massachusetts Institute of Technology, Cambridge, MA (A.Y., J.K., M.K.); Department of Pathology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA ..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Janka","family":"Kisucka","sequence":"additional","affiliation":[{"name":"From the Immune Disease Institute (A.B., S.F.D.M., T.A.F., D.D.W.), Program in Cellular and Molecular Medicine, Children\u2019s Hospital Boston (A.B., S.F.D.M., T.A.F., D.D.W.), and Department of Pediatrics (A.B., S.F.D.M., T.A.F., D.D.W.), Harvard Medical School, Boston, MA; Biology Department, Massachusetts Institute of Technology, Cambridge, MA (A.Y., J.K., M.K.); Department of Pathology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA ..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tobias A.","family":"Fuchs","sequence":"additional","affiliation":[{"name":"From the Immune Disease Institute (A.B., S.F.D.M., T.A.F., D.D.W.), Program in Cellular and Molecular Medicine, Children\u2019s Hospital Boston (A.B., S.F.D.M., T.A.F., D.D.W.), and Department of Pediatrics (A.B., S.F.D.M., T.A.F., D.D.W.), Harvard Medical School, Boston, MA; Biology Department, Massachusetts Institute of Technology, Cambridge, MA (A.Y., J.K., M.K.); Department of Pathology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA ..."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Olivier","family":"Kocher","sequence":"additional","affiliation":[{"name":"From the Immune Disease Institute (A.B., S.F.D.M., T.A.F., D.D.W.), Program in Cellular and Molecular Medicine, Children\u2019s Hospital Boston (A.B., S.F.D.M., T.A.F., D.D.W.), and Department of Pediatrics (A.B., S.F.D.M., T.A.F., D.D.W.), Harvard Medical School, Boston, MA; Biology Department, Massachusetts Institute of Technology, Cambridge, MA (A.Y., J.K., M.K.); Department of Pathology and Center for Vascular Biology Research, Beth Israel Deaconess Medical Center, Harvard Medical School, Boston, MA 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