CD39-Diannexin alleviates the platelet storage lesion by protecting platelets from activation, a new attempt from a traditional perspective.

Due to platelet storage lesions (PSL), transfused platelets are unable to function properly in the prevention and treatment of bleeding in critically ill patients. It is a traditional assumption that PSL is closely related to platelet activation during storage because of the exposure of CD62P, phosphatidylserine (PS), etc. In this standpoint, activated platelets in vitro cannot be reactivated in vivo to exert their hemostatic function and exposed PS accelerates platelet clearance. Therefore, reducing platelet activation is helpful to alleviate PSL. Diannexin is the dimer of annexin that has a higher affinity for PS. CD39 is an ADP hydrolase produced by the vascular endothelium. As a result, we construct CD39-Diannexin (CD39-DA) fusion protein and hypothesize that CD39-DA can reduce platelet activation during storage to alleviate PSL. CD39-DA can bind to the exposed PS on the surface of stored platelets by immunofluorescence. Compared to the control groups, CD39-DA reserves part of stored platelets' aggregation function confirmed by platelet aggregation assay, induced by AA, ADP and collagen. Additionally, CD39-DA reduces lactic dehydrogenase (LDH) levels and CD62P-positive events after three-day storage. Interestingly, we preliminarily discover that CD39-DA may reduce stored platelets' apoptosis and increase aggregatory platelets after activation by thrombin, collagen and calcium, which is marked by GSAO. In conclusion, we confirm that CD39-DA can alleviate PSL by reducing platelet activation.