title: Mice lacking the SLAM family member CD84 display unaltered platelet function in hemostasis and thrombosis.
abstract: BACKGROUND
  Platelets are anuclear cell fragments derived from bone marrow megakaryocytes that safeguard vascular integrity by forming thrombi at sites of vascular injury. Although the early events of thrombus formation--platelet adhesion and aggregation--have been intensively studied, less is known about the mechanisms and receptors that stabilize platelet-platelet interactions once a thrombus has formed. One receptor that has been implicated in this process is the signaling lymphocyte activation molecule (SLAM) family member CD84, which can undergo homophilic interactions and becomes phosphorylated upon platelet aggregation.
  
  
  OBJECTIVE
  The role of CD84 in platelet physiology and thrombus formation was investigated in CD84-deficient mice.
  
  
  RESULTS
  We generated CD84-deficient mice and analyzed their platelets in vitro and in vivo. Cd84(-/-) platelets exhibited normal activation and aggregation responses to classical platelet agonists. Furthermore, CD84 deficiency did not affect integrin-mediated clot retraction and spreading of activated platelets on fibrinogen. Notably, also the formation of stable three-dimensional thrombi on collagen-coated surfaces under flow ex vivo was unaltered in the blood of Cd84(-/-) mice. In vivo, Cd84(-/-) mice exhibited unaltered hemostatic function and arterial thrombus formation.
  
  
  CONCLUSIONS
  These results show that CD84 is dispensable for thrombus formation and stabilization, indicating that its deficiency may be functionally compensated by other receptors or that it may be important for platelet functions different from platelet-platelet interactions.
authors.affiliation: University of Würzburg, Department of Experimental Biomedicine, University Hospital and Rudolf Virchow Center, Würzburg, Germany.
authors.forename: Sebastian
authors.initials: S
authors.lastname: Hofmann
authors.affiliation: University of Würzburg, Department of Experimental Biomedicine, University Hospital and Rudolf Virchow Center, Würzburg, Germany.
authors.forename: Attila
authors.initials: A
authors.lastname: Braun
authors.affiliation: University of Würzburg, Department of Experimental Biomedicine, University Hospital and Rudolf Virchow Center, Würzburg, Germany.
authors.forename: Rastislav
authors.initials: R
authors.lastname: Pozgaj
authors.affiliation: University of Würzburg, Department of Experimental Biomedicine, University Hospital and Rudolf Virchow Center, Würzburg, Germany.
authors.forename: Martina
authors.initials: M
authors.lastname: Morowski
authors.affiliation: University of Würzburg, Department of Experimental Biomedicine, University Hospital and Rudolf Virchow Center, Würzburg, Germany.
authors.forename: Timo
authors.initials: T
authors.lastname: Vögtle
authors.affiliation: University of Würzburg, Department of Experimental Biomedicine, University Hospital and Rudolf Virchow Center, Würzburg, Germany.
authors.forename: Bernhard
authors.initials: B
authors.lastname: Nieswandt
mesh_terms: D000818:Animals; D015703:Antigens, CD / Q000235:genetics* / Q000378:metabolism*; D001792:Blood Platelets / Q000502:physiology*; D003593:Cytoplasm / Q000378:metabolism; D055786:Gene Knockout Techniques; D006487:Hemostasis; D051379:Mice; D010641:Phenotype; D010766:Phosphorylation; D010973:Platelet Adhesiveness; D010974:Platelet Aggregation; D000071176:Signaling Lymphocytic Activation Molecule Family; D013927:Thrombosis / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D015703:Antigens, CD; C498971:Cd84 protein, mouse; D000071176:Signaling Lymphocytic Activation Molecule Family