Desialylation accelerates platelet clearance after refrigeration and initiates GPIbα metalloproteinase-mediated cleavage in mice.
作者： A. J. Gerard Jansen , Emma C. Josefsson , Viktoria Rumjantseva , Qiyong Peter Liu , Hervé Falet
DOI: 10.1182/BLOOD-2011-05-355628
关键词:
摘要: When refrigerated platelets are rewarmed, they secrete active sialidases, including the lysosomal sialidase Neu1, and express surface Neu3 that remove sialic acid from platelet von Willebrand factor receptor (VWFR), specifically GPIbα subunit. The recovery circulation of is greatly improved by storage in presence inhibitors sialidases. Desialylated VWFR also a target for metalloproteinases (MPs), because GPV cleaved platelets. Receptor shedding inhibited MP inhibitor GM6001 does not occur Adam17ΔZn/ΔZn expressing inactive ADAM17. Critically, desialylation absence MP-mediated sufficient to cause rapid clearance circulation. Desialylation therefore triggers primes MP-dependent cleavage.
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