{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,16]],"date-time":"2026-09-16T02:05:45Z","timestamp":1789524345502,"version":"build-2803163510"},"reference-count":62,"publisher":"American Society of Hematology","issue":"18","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2025,5,1]]},"abstract":"<jats:sec>\n                    <jats:title>Abstract<\/jats:title>\n                    <jats:p>Antibodies to \u03b22-glycoprotein I (\u03b22GPI) cause thrombosis in antiphospholipid syndrome; however, the role of \u03b22GPI in coagulation in\u00a0vivo is not understood. To address this issue, we developed \u03b22GPI-deficient mice (Apoh\u2013\/\u2013) by deleting exons 2 and 3 of Apoh using CRISPR\/Cas9 and compared the development of thrombosis in wild-type (WT) and Apoh\u2013\/\u2013 mice using rose bengal\u2013 and FeCl3-induced carotid thrombosis, laser-induced cremaster arteriolar injury, and inferior vena cava (IVC) stasis models. We also compared tail bleeding times and activation of platelets from WT and Apoh\u2013\/\u2013 mice in the absence and presence of \u03b22GPI. Apoh\u2013\/\u2013 mice demonstrated prolonged time to occlusion of the carotid after exposure to rose bengal or FeCl3 and reduced platelet and fibrin accumulation in cremasteric arterioles after laser injury. Significantly smaller thrombi formed in the IVC of Apoh\u2013\/\u2013 mice 48 hours after IVC occlusion. The activated partial thromboplastin time and prothrombin time, as well as activated partial thromboplastin time reagent and tissue factor\u2013induced thrombin generation times, of Apoh\u2013\/\u2013 and WT plasma revealed no differences. However, we observed significant prolongation of tail bleeding in Apoh\u2013\/\u2013 mice and reduced P-selectin expression and fibrinogen binding to activated \u03b12b\u03b23 on platelets from these mice after stimulation with thrombin; these changes were reversed by \u03b22GPI. A protease activated receptor 3 (PAR3) antibody blocked thrombin-induced activation of WT platelets and the ability of \u03b22GPI to restore thrombin-induced activation of Apoh\u2013\/\u2013 platelets. These studies demonstrate that \u03b22GPI may promote platelet activation by enhancing the ability of PAR3 to present thrombin to PAR4.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1182\/blood.2024024469","type":"journal-article","created":{"date-parts":[[2025,1,27]],"date-time":"2025-01-27T15:59:23Z","timestamp":1737993563000},"page":"2086-2099","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":8,"title":["Protection of \u03b22GPI-deficient mice from thrombosis reflects a defect in PAR3-facilitated platelet activation"],"prefix":"10.1182","volume":"145","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-9108-0485","authenticated-orcid":false,"given":"Paresh P.","family":"Kulkarni","sequence":"first","affiliation":[{"name":"1Department of Cardiovascular and Metabolic Sciences, Cleveland Clinic, Cleveland, OH"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ravi 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