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Background  Two congenital bleeding diatheses have been identified in Thoroughbred horses: Glanzmann thrombasthenia (GT) and a second, novel diathesis associated with abnormal platelet function in response to collagen and thrombin stimulation.    Hypothesis/Objectives  Platelet dysfunction in horses with this second thrombasthenia results from a secretory defect.    Animals  Two affected and 6 clinically normal horses.    Methods  Ex vivo study. Washed platelets were examined for (1) expression of the α II b‐β3 integrin; (2) fibrinogen binding capacity in response to  ADP  and thrombin; (3) secretion of dense and α‐granules; (4) activation of the mammalian target of rapamycin ( mTOR )‐protein kinase B ( AKT ) signaling pathway; and (5) cellular distribution of phosphatidylinositol‐4‐phosphate‐3‐kinase, class 2B ( PIK 3C2B) and  SH 2 containing inositol‐5′‐phosphatase 1 ( SHIP 1).    Results  Platelets from affected horses expressed normal amounts of α II b‐β3 integrin and bound fibrinogen normally in response to  ADP , but bound 80% less fibrinogen in response to thrombin. α‐granules only released 50% as much Factor V as control platelets, but dense granules released their contents normally. Protein kinase B (AKT) phosphorylation was reduced after thrombin activation, but  mTOR  Complex 2 ( mTORC 2) and phosphoinositide‐dependent kinase 1 (PDK1) signaling were normal. SH2‐containing inositol‐5'‐phosphatase 1 (SHIP1) did not localize to the cytoskeleton of affected platelets and was decreased overall consistent with reduced  AKT  phosphorylation.    Conclusions and clinical significance  Defects in fibrinogen binding, granule secretion, and signal transduction are unique to this thrombasthenia, which we designate as atypical equine thrombasthenia.

Association of Factor V Secretion with Protein Kinase B Signaling in Platelets from Horses with Atypical Equine Thrombasthenia