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Apolipoprotein A-I, elevated in trauma patients, inhibits platelet activation and decreases clot strength.
Jones, Wilbert L; Ramos, Christopher R; Banerjee, Anirban; Moore, Ernest E; Hansen, Kirk C; Coleman, Julia R; Kelher, Marguerite; Neeves, Keith B; Silliman, Christopher C; Di Paola, Jorge; Branchford, Brian.
Afiliación
  • Jones WL; Departments of Surgery, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Ramos CR; Departments of Surgery, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Banerjee A; Departments of Surgery, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Moore EE; Departments of Surgery, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Hansen KC; Department of Surgery, Denver Health Medical Center, Denver, CO, USA.
  • Coleman JR; Department of Biochemistry/Molecular Genetics, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Kelher M; Departments of Surgery, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Neeves KB; Departments of Surgery, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Silliman CC; Department of Bioengineering, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Di Paola J; Department of Pediatrics, School of Medicine University of Colorado Denver, Anschutz Medical Campus, Aurora, CO, USA.
  • Branchford B; Vitalant Research Institute, Vitalant Mountain Division, Denver, CO, USA.
Platelets ; 33(8): 1119-1131, 2022 Nov 17.
Article en En | MEDLINE | ID: mdl-35659185
Apolipoprotein A-I (ApoA-I) is elevated in the plasma of a subgroup of trauma patients with systemic hyperfibrinolysis. We hypothesize that apoA-I inhibits platelet activation and clot formation. The effects of apoA-I on human platelet activation and clot formation were assessed by whole blood thrombelastography (TEG), platelet aggregometry, P-selectin surface expression, microfluidic adhesion, and Akt phosphorylation. Mouse models of carotid artery thrombosis and pulmonary embolism were used to assess the effects of apoA-I in vivo. The ApoA-1 receptor was investigated with transgenic mice knockouts (KO) for the scavenger receptor class B member 1 (SR-BI). Compared to controls, exogenous human apoA-I inhibited arachidonic acid and collagen-mediated human and mouse platelet aggregation, decreased P-selectin surface expression and Akt activation, resulting in diminished clot strength and increased clot lysis by TEG. ApoA-I also decreased platelet aggregate size formed on a collagen surface under flow. In vivo, apoA-I delayed vessel occlusion in an arterial thrombosis model and conferred a survival advantage in a pulmonary embolism model. SR-BI KO mice significantly reduced apoA-I inhibition of platelet aggregation versus wild-type platelets. Exogenous human apoA-I inhibits platelet activation, decreases clot strength and stability, and protects mice from arterial and venous thrombosis via the SR-BI receptor.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Embolia Pulmonar / Trombosis Límite: Animals / Humans Idioma: En Revista: Platelets Asunto de la revista: HEMATOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido
Texto completo
Añadir a Mi BVS
Imprimir
XML
PubMed Links
Buscar en Google

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Embolia Pulmonar / Trombosis Límite: Animals / Humans Idioma: En Revista: Platelets Asunto de la revista: HEMATOLOGIA Año: 2022 Tipo del documento: Article País de afiliación: Estados Unidos Pais de publicación: Reino Unido