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巨核细胞运动性与血小板生成

Megakaryocyte motility and platelet formation.

作者信息

Leven R M

机构信息

Division of Biology and Medicine, Lawrence Berkeley Laboratory, University of California, Berkeley 94720.

出版信息

Scanning Microsc. 1987 Dec;1(4):1701-9.

PMID:3324324
Abstract

The mechanism of platelet formation is reviewed with special emphasis on the role of the cytoskeleton. The three major theories for platelet formation are by cytoplasmic budding, cytoplasmic dissolution or pseudopod formation. Most evidence indicates that platelets form as fragments of megakaryocyte pseudopodia. Pseudopodia formation is stimulated in vitro by thrombocytopenic rabbit plasma. It is inhibited by vincristine and altered by taxol. Cytochalasins cause pseudopodia to form in isolated megakaryocytes. Therefore, normal pseudopodia formation may depend on a combination of microfilament disorganization and microtubule elongation.

摘要

本文综述了血小板形成的机制,特别强调了细胞骨架的作用。血小板形成的三种主要理论是通过细胞质出芽、细胞质溶解或伪足形成。大多数证据表明,血小板是作为巨核细胞伪足的片段形成的。体外血小板减少的兔血浆可刺激伪足形成。它被长春新碱抑制,并被紫杉醇改变。细胞松弛素可使分离的巨核细胞形成伪足。因此,正常的伪足形成可能依赖于微丝解聚和微管伸长的共同作用。

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