Shedding light on GPIbα shedding

Purpose of reviewEctodomain shedding has been investigated since the late 1980s. The abundant and platelet specific GPIb alpha receptor is cleaved by ADAM17 resulting in the release of its ectodomain called glycocalicin. This review will address the role of glycocalicin as an end-stage marker of platelet turnover and storage lesion and will consider a potential function as effector in processes beyond hemostasis.Recent findingsGlycocalicin has been described as a marker for platelet senescence, turnover and storage lesion but is not routinely used in a clinical setting because its diagnostic value is nondiscriminatory. Inhibition of glycocalicin shedding improves posttransfusion recovery but little is known (yet) about potential hemostatic improvements. In physiological settings, GPIb alpha shedding is restricted to the intracellular GPIb alpha receptor subpopulation suggesting a role for shedding or glycocalicin beyond hemostasis.SummarySo far, all evidence represents glycocalicin as an end-stage biomarker of platelet senescence and a potential trigger for platelet clearance. The extensive list of interaction partners of GPIb alpha in fields beyond hemostasis opens new possibilities to investigate specific effector functions of glycocalicin.