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Blood. 2018 Oct 22. pii: blood-2018-03-742668. doi: 10.1182/blood-2018-03-742668. [Epub ahead of print]

Mechanisms of receptor shedding in platelets.

Author information

1
ACRF Department of Cancer Biology and Therapeutics, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia.
2
Australian Centre for Blood Diseases, Monash University, Melbourne, VIC, Australia.
3
ACRF Department of Cancer Biology and Therapeutics, The John Curtin School of Medical Research, The Australian National University, Canberra, ACT, Australia; elizabeth.gardiner@anu.edu.au.

Abstract

The ability to up- and down-regulate surface exposed proteins and receptors is a powerful process that allows a cell to instantly respond to its microenvironment. In particular, mobile cells in the bloodstream must rapidly react to conditions where infection or inflammation are detected, and become proadhesive, phagocytic and/or procoagulant. Platelets are one such blood cell that must rapidly acquire and manage proadhesive and procoagulant properties in order to execute their primary function in hemostasis. The regulation of platelet membrane properties is achieved via several mechanisms, one of which involves the controlled metalloproteolytic release of adhesion receptors and other proteins from the platelet surface. Proteolysis effectively lowers receptor density and reduces the reactivity of platelets, and is a mechanism to control robust platelet activation. Recent research has also established clear links between levels of platelet receptors and platelet lifespan. In this review we will discuss the current knowledge of metalloproteolytic receptor regulation in the vasculature with emphasis on the platelet receptor system, to highlight how receptor density can influence both platelet function and platelet survival.

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