{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,12]],"date-time":"2026-11-12T21:34:09Z","timestamp":1794519249161,"version":"4.9.1"},"reference-count":84,"publisher":"American Society of Hematology","issue":"16","content-domain":{"domain":["ashpublications.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2024,10,17]]},"abstract":"<jats:sec>\n                  <jats:title>Abstract<\/jats:title>\n                  <jats:p>Patients with thrombocytopenia require platelet transfusion to prevent and stop hemorrhage. Cold storage of platelets results in complex molecular lesions, including changes in membrane microdomains that are recognized by host macrophages and hepatocyte counter-receptors, resulting in phagocytosis and clearance upon transfusion. For this reason, platelets are stored at room temperature, a method that confers increased risk of bacterial contamination. By applying signaling analysis and genetic and pharmacological approaches, we identified that cold-induced activation of RAS homolog family, member A (RHOA) GTPase causes the major hallmarks of platelet cold storage lesions. RHOA deficiency renders murine platelets insensitive to cold storage\u2013induced damage, and pharmacological inhibition by a RHOA activation inhibitor, R-G04, can prevent the cold storage\u2013induced lesions. RHOA inhibition prevents myosin activation and clathrin-independent formation and internalization of lipid rafts enriched in active glycosyltransferases as well as abnormal distribution of GPIb\u03b1. RHOA inhibition further prevents the metabolic reprogramming of cold storage\u2013induced lesions and allows the maintenance of glycolytic flux and mitochondria-dependent respiration. Importantly, human platelets transfused in mice after cold storage, in the presence of R-G04 or its more potent enantiomer S-G04, can circulate in\u00a0vivo at similar levels as room temperature\u2013stored platelets while retaining their hemostatic activity in\u00a0vivo, as assessed by bleeding time correction in aspirin-treated mice. Our studies provide a mechanism-based translational approach to prevent cold storage\u2013induced damage, which is useful for human platelet transfusion in patients with thrombocytopenia.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1182\/blood.2023021453","type":"journal-article","created":{"date-parts":[[2024,8,1]],"date-time":"2024-08-01T19:53:48Z","timestamp":1722542028000},"page":"1732-1746","update-policy":"https:\/\/doi.org\/10.1182\/blood.2019cm0000","source":"Crossref","is-referenced-by-count":23,"title":["Inhibition of RHOA activity preserves the survival and hemostasis function of long-term cold-stored platelets"],"prefix":"10.1182","volume":"144","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-8228-9570","authenticated-orcid":false,"given":"Shailaja","family":"Hegde","sequence":"first","affiliation":[{"name":"1Hoxworth Blood Center, University of Cincinnati College of Medicine, Cincinnati, OH"},{"name":"2Division of Experimental Hematology and Cancer Biology, 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