Potential mechanisms of clearance of long-term cold-stored murine platelets from the circulation. Long-term cold-stored platelets undergo clustering of the platelet GP complex (Ibαβ-IX)2-V, resulting in the recognition of exposed β-N-acetylglucosamine residues by αMβ2 receptors on hepatic macrophages and phagocytosis. It has been also reported that with long-term cold storage, galactose residues cluster sufficiently to induce recognition by hepatocyte asialoglycoprotein (ASGP) receptors and subsequent phagocytosis. The shedding of GP Ibα and GPV due to metalloproteinase ADAM17 activity observed during prolonged cold storage and rewarming is associated with a reduced survival of platelets in the circulation, although the implicated mechanisms have not been fully elucidated. Illustration by Kenneth Probst.

Potential mechanisms of clearance of long-term cold-stored murine platelets from the circulation. Long-term cold-stored platelets undergo clustering of the platelet GP complex (Ibαβ-IX)2-V, resulting in the recognition of exposed β-N-acetylglucosamine residues by αMβ2 receptors on hepatic macrophages and phagocytosis. It has been also reported that with long-term cold storage, galactose residues cluster sufficiently to induce recognition by hepatocyte asialoglycoprotein (ASGP) receptors and subsequent phagocytosis. The shedding of GP Ibα and GPV due to metalloproteinase ADAM17 activity observed during prolonged cold storage and rewarming is associated with a reduced survival of platelets in the circulation, although the implicated mechanisms have not been fully elucidated. Illustration by Kenneth Probst.

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