蛋白质糖基化在血小板计数与功能调控中作用的研究现状

Research status on role of protein glycosylation in platelet count and function regulation

糖蛋白上的聚糖是细胞黏附和细胞间通讯的主要参与者, 糖基化通过调节血小板膜糖蛋白影响血小板数量和功能。在糖基转移酶(GT)的作用下, 巨核细胞表面蛋白的糖基化参与调控巨核细胞成熟、分化和血小板生成。血小板去唾液酸化后, 被相关受体识别而快速清除, 并触发级联信号介导血小板生成素(TPO)产生, 从而完成对血小板数量的快速调控。血小板膜糖蛋白多个糖基化关键位点的改变影响其与配体的结合能力, 这也提示糖基化对血小板功能发挥具有重要作用。病理状态下, 蛋白质糖基化异常, 可导致血小板数量异常和功能紊乱, 从而引起相关疾病。笔者拟就蛋白质糖基化对血小板数量和功能的调控机制进行阐述, 旨在进一步了解蛋白质糖基化在血小板增多、减少和功能异常中的作用。

Glycans on glycoproteins are major participants in cell adhesion and intercellular communication,and glycosylation affects platelet count and function by regulating platelet membrane glycoproteins.Under the function of glycosyltransferases(GT),glycosylation of megakaryocyte surface proteins is involved in the regulation of megakaryocyte maturation,differentiation and thrombopoiesis.Meanwhile,desialylation of platelets allows them to be recognized by relevant receptors for rapid clearance,and triggers cascade signals that mediate the production of thrombopoietin(TPO),resulting in the rapid regulation of platelet count.Alteration of several key glycosylation sites of platelet membrane glycoproteins affects their ability to bind ligands,also suggests that glycosylation plays an important role in platelet function.In pathological conditions,abnormalities in glycosylation can lead to abnormal counts and dysfunctions of platelet causing related diseases.This article intends to state the regulatory mechanisms of protein glycosylation on platelet count and function,in order to provide further insights into the role of protein glycosylation in platelet increase/decrease and dysfunction under disease conditions.