Mechanistic insight into the procoagulant activity of tumor-derived apoptotic vesicles.

摘要: Abstract Background Chemotherapy induces the release of apoptotic vesicles (ApoV) from tumor plasma membrane. Tumor ApoV may enhance risk thrombotic events in cancer patients undergoing chemotherapy. However, relative contribution to coagulation and pathways involved remain poorly characterized. In addition, this study sets out compare procoagulant activity chemotherapy-induced with their cell origin determine mechanisms ApoV-induced coagulation. Methods We utilized human murine lines chemotherapeutic agents requirement for factors (tissue factor; TF, FII, FV, FVII, FVIII, FIX phosphatidylserine) ApoV. The role previously identified ApoV-associated FV was determined a functional assay. Results were significantly more per microgram protein compared parental living or dying cells. phase peak fibrin generation, dependent on phosphatidylserine, TF expression, FVII prothrombinase complex. intrinsic FVIII dispensable. could not support absence supplied, exogenous FV. Conclusions are than require extrinsic tenase complex activate early Endogenous is serum-derived functional, but non-essential ApoV-mediated generation. General significance This clarifies released