In:
Vox Sanguinis, Wiley, Vol. 111, No. 3 ( 2016-10), p. 247-256
Abstract:
In mice, loss of sialic acid resulting in shedding of glycoprotein ( GP ) Ibα and GPV has been linked to platelet survival. The aim of this study was to determine whether loss of sialic acid and the GPI b‐ IX ‐V complex contributes to development of the platelet storage lesion ( PSL ) in human platelet concentrates ( PC s). Materials and methods PC s (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 GPI b‐ IX ‐V complex, CD 62P, surface glycans and PS exposure. The functionality of stored platelets was determined employing aggregometry and ristocetin‐induced VWF binding. Results Storage time of PC s in blood banks is limited to 7 days. During this time period, a minor but gradually increasing subpopulation of GPI bα‐negative platelets was observed. Also, ristocetin‐induced VWF binding was impaired in a small population of platelets. Mean surface expression of GPI bα and GPV remained stable until day 9, whereas CD 62P expression increased; also a rapid decrease in ADP ‐induced aggregation was observed for PAS ‐C, PAS ‐E and Mirasol‐treated PC s. Upon prolonged storage ( 〉 9 days), a slow decline in surface expression of GPI bα 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 GPI bα occur from day 2 onwards. Loss of sialic acid and subsequent shedding of GPI bα and GPV is not an early event during the development of the PSL .
Type of Medium:
Online Resource
ISSN:
0042-9007
,
1423-0410
DOI:
10.1111/vox.2016.111.issue-3
Language:
English
Publisher:
Wiley
Publication Date:
2016
detail.hit.zdb_id:
1483587-3
detail.hit.zdb_id:
80313-3
