Transfusion Research Center, Belgian Red Cross Flanders.
Faculty of Medicine and Health Sciences, Ghent University, Ghent, Belgium.
Curr Opin Hematol. 2024 Sep 1;31(5):224-229. doi: 10.1097/MOH.0000000000000826. Epub 2024 May 9.
Ectodomain shedding has been investigated since the late 1980s. The abundant and platelet specific GPIbα 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.
Glycocalicin 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, GPIbα shedding is restricted to the intracellular GPIbα receptor subpopulation suggesting a role for shedding or glycocalicin beyond hemostasis.
So 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 GPIbα in fields beyond hemostasis opens new possibilities to investigate specific effector functions of glycocalicin.
自从 20 世纪 80 年代末以来，人们一直在研究细胞外结构域脱落。丰富的血小板特异性 GPIbα 受体被 ADAM17 切割，导致其细胞外结构域即糖蛋白 Ibα（glycocalicin）释放。这篇综述将讨论糖蛋白 Ibα 作为血小板更新和储存损伤的终末标志物的作用，并将考虑其作为止血以外过程中的效应因子的潜在功能。
糖蛋白 Ibα 已被描述为血小板衰老、更新和储存损伤的标志物，但由于其诊断价值没有特异性，尚未在临床常规应用。糖蛋白 Ibα 脱落的抑制可改善输注后的恢复，但对潜在的止血改善知之甚少（尚）。在生理状态下，GPIbα 的脱落仅限于细胞内 GPIbα 受体亚群，提示脱落或糖蛋白 Ibα 具有止血以外的作用。
到目前为止，所有证据都将糖蛋白 Ibα 作为血小板衰老的终末生物标志物和血小板清除的潜在触发物。GPIbα 在止血以外的领域与广泛的相互作用伙伴的列表为研究糖蛋白 Ibα 的特定效应功能开辟了新的可能性。
