Evaluation of the role of the GPIb-IX-V receptor complex in development of the platelet storage lesion

Background and Objectives In mice, loss of sialic acid resulting in shedding of glycoprotein (GP) Ib alpha and GPV has been linked to platelet survival. The aim of this study was to determine whether loss of sialic acid and the GPIb-IX-V complex contributes to development of the platelet storage lesion (PSL) in human platelet concentrates (PCs). Materials and methods PCs (stored in plasma (with or without Mirasol treatment); PAS-C or PAS-E) were stored at room temperature. Flow cytometry was used to monitor membrane expression of the GPIb-IX-V complex, CD62P, surface glycans and PS exposure. The functionality of stored platelets was determined employing aggregometry and ristocetin-induced VWF binding. Results Storage time of PCs in blood banks is limited to 7 days. During this time period, a minor but gradually increasing subpopulation of GPIb alpha-negative platelets was observed. Also, ristocetin-induced VWF binding was impaired in a small population of platelets. Mean surface expression of GPIb alpha and GPV remained stable until day 9, whereas CD62P expression increased; also a rapid decrease in ADP-induced aggregation was observed for PAS-C, PAS-E and Mirasol-treated PCs. Upon prolonged storage (>9 days), a slow decline in surface expression of GPIba and GPV was observed; no major changes were observed in surface sialylation with the exception of Mirasol-treated platelets. Conclusion In a small population of stored platelets, changes in GPIba occur from day 2 onwards. Loss of sialic acid and subsequent shedding of GPIba and GPV is not an early event during the development of the PSL.