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To determine the effect of <jats:styled-content style=\"fixed-case\">SCD<\/jats:styled-content> on atherosclerosis and thrombosis, mice with <jats:styled-content style=\"fixed-case\">SCD<\/jats:styled-content> along with controls were generated by transplantation of bone marrow from mice carrying the homozygous sickle cell mutation (<jats:italic>Hbb<\/jats:italic><jats:sup><jats:italic>h\u03b2s\/h\u03b2s<\/jats:italic><\/jats:sup>) or wild\u2010type mice (<jats:italic>Hbb<\/jats:italic><jats:sup><jats:italic>+\/+<\/jats:italic><\/jats:sup>) into C57<jats:styled-content style=\"fixed-case\">BL<\/jats:styled-content>6\/J or apolipoprotein E deficient (<jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup>) recipient mice. At the time of sacrifice, 23\u201328\u00a0weeks following bone marrow transplantation, anaemia, reticulocytosis, and splenomegaly were present in mice receiving <jats:italic>Hbb<\/jats:italic><jats:sup><jats:italic>h\u03b2s\/h\u03b2s<\/jats:italic><\/jats:sup> bone marrow compared with control mice. Analysis of atherosclerosis involving the aortic root revealed reduced atherosclerotic lesion area with reduced macrophage content and increased collagen content in <jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>, Hbb<\/jats:italic><jats:sup><jats:italic>h\u03b2s\/h\u03b2s<\/jats:italic><\/jats:sup> mice compared to <jats:italic>Apoe<\/jats:italic><jats:sup><jats:italic>\u2212\/\u2212<\/jats:italic><\/jats:sup><jats:italic>, Hbb<\/jats:italic><jats:sup><jats:italic>+\/+<\/jats:italic><\/jats:sup> mice. In a carotid thrombosis model, the time to thrombosis was prolonged in <jats:italic>Hbb<\/jats:italic><jats:sup><jats:italic>h\u03b2s\/h\u03b2s<\/jats:italic><\/jats:sup> mice compared to <jats:italic>Hbb<\/jats:italic><jats:sup><jats:italic>+\/+<\/jats:italic><\/jats:sup> mice. This apparent protective effect of <jats:styled-content style=\"fixed-case\">SCD<\/jats:styled-content> on atherosclerosis and thrombosis was diminished by inhibition of heme oxygenase\u20101 (<jats:styled-content style=\"fixed-case\">HMOX<\/jats:styled-content>1) using zinc protoporphyrin <jats:styled-content style=\"fixed-case\">IX<\/jats:styled-content>.<\/jats:p><jats:p>We conclude that <jats:styled-content style=\"fixed-case\">SCD<\/jats:styled-content> in mice is paradoxically protective against atherosclerosis and thrombosis, highlighting the complexity of vascular events in <jats:styled-content style=\"fixed-case\">SCD<\/jats:styled-content>. This protective effect is at least partially mediated by induction of <jats:styled-content style=\"fixed-case\">HMOX<\/jats:styled-content>1.<\/jats:p>","DOI":"10.1111\/bjh.12342","type":"journal-article","created":{"date-parts":[[2013,4,17]],"date-time":"2013-04-17T11:59:05Z","timestamp":1366199945000},"page":"120-129","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":23,"title":["Paradoxical protection from atherosclerosis and thrombosis in a mouse model of sickle cell disease"],"prefix":"10.1111","volume":"162","author":[{"given":"Hui","family":"Wang","sequence":"first","affiliation":[{"name":"Department of Internal Medicine Cardiovascular Research Center University of Michigan Ann Arbor MI USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Luo","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Cardiovascular Research Center University of Michigan Ann Arbor MI 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