Expression profiling of platelets from young (3 months) homozygous Jak2 R1063H mice and wild-type controls

Patients with myeloproliferative neoplasms (MPN), are known to be at an elevated risk for thrombosis but the mechanism for MPN-related coagulation activation is not yet fully characterized. While increased hematocrit has been re-evaluated as a contributing factor, additional mechanisms such as chronic inflammation and a pro-adhesive phenotype associated with increased endothelial P-selectin expression have been elucidated in MPN thrombogenesis. Additionally, non-myeloid inflammatory cells, red blood cells and platelets may also contribute to increased vascular resistance and promote thrombosis. However, the mechanism of thrombosis associated with JAK2 germline mutations has not been described. We performed expression gene profiling of platelets isolated from young (3 months) homozygous Jak2 R1063H mice and wild-type controls.