Servicio de Hematología y Oncología Médica, Centro Regional de Hemodonación, Hospital Universitario Morales Meseguer, IMIB-Arrixaca, Red CIBERER CB15/00055, 30003 Murcia, Spain.
Grado de Medicina, Universidad Católica San Antonio (UCAM), Campus de los Jerónimos, 30107 Murcia, Spain.
Int J Mol Sci. 2019 Jul 16;20(14):3484. doi: 10.3390/ijms20143484.
Platelets are anuclear cells with a short lifespan that play an essential role in many pathophysiological processes, including haemostasis, inflammation, infection, vascular integrity, and metastasis. Billions of platelets are produced daily from megakaryocytes (platelet precursors). Despite this high production, the number of circulating platelets is stable and, under resting conditions, they maintain their typical discoid shape thanks to cytoskeleton proteins. The activation of platelets is associated with dynamic and rapid changes in the cytoskeleton. Two cytoskeletal polymer systems exist in megakaryocytes and platelets: actin filaments and microtubules, based on actin, and α- and β-tubulin heterodimers, respectively. Herein, we will focus on platelet-specific tubulins and their alterations and role of the microtubules skeleton in platelet formation (thrombopoiesis). During this process, microtubules mediate elongation of the megakaryocyte extensions (proplatelet) and granule trafficking from megakaryocytes to nascent platelets. In platelets, microtubules form a subcortical ring, the so-called marginal band, which confers the typical platelet discoid shape and is also responsible for changes in platelet morphology upon activation. Molecular alterations in the gene encoding β1 tubulin and microtubules post-translational modifications may result in quantitative or qualitative changes in tubulin, leading to altered cytoskeleton reorganization that may induce changes in the platelet number (thrombocytopenia), morphology or function. Consequently, β1-tubulin modifications may participate in pathological and physiological processes, such as development.
血小板是一种无核细胞，寿命较短，但在许多病理生理过程中起着至关重要的作用，包括止血、炎症、感染、血管完整性和转移。每天有数十亿个血小板由巨核细胞（血小板前体）产生。尽管产量如此之高，但循环血小板的数量仍然保持稳定，在休息状态下，由于细胞骨架蛋白的存在，它们保持典型的圆盘形状。血小板的激活与细胞骨架的动态和快速变化有关。巨核细胞和血小板中有两种细胞骨架聚合物系统：基于肌动蛋白的肌动蛋白丝和微管，以及α和β-微管蛋白异二聚体。在此，我们将重点介绍血小板特异性微管及其改变以及微管骨架在血小板形成（血小板生成）中的作用。在此过程中，微管介导巨核细胞延伸（血小板前体）的伸长和颗粒从巨核细胞向新生血小板的运输。在血小板中，微管形成一个亚皮质环，即所谓的边缘带，赋予血小板典型的圆盘形状，并负责血小板激活时形态的变化。β1 微管蛋白编码基因的分子改变和微管的翻译后修饰可能导致微管的定量或定性变化，导致细胞骨架重新排列的改变，从而可能导致血小板数量（血小板减少症）、形态或功能的改变。因此，β1 微管蛋白的修饰可能参与病理和生理过程，如发育。
