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Rac1 GTP酶控制髓鞘形成和脱髓鞘过程。

Rac1 GTPase controls myelination and demyelination.

作者信息

Park Hwan Tae, Feltri M Laura

机构信息

Department of Physiology; Mitochondria Hub Regulation Center (MHRC); College of Medicine; Dong-A University; Busan, South Korea.

出版信息

Bioarchitecture. 2011 May;1(3):110-113. doi: 10.4161/bioa.1.3.16985.

Abstract

After peripheral nerve injuries, Wallerian degeneration starts with a stereotypic fragmentation of myelin sheath into myelin ovoids, which occur near Schmidt-Lantermann incisures (SLI). This demyelination process requires a dramatic change in cytoskeletal structures in Schwann cells. We have recently shown that actin polymerization around SLI is an important step for cleavage of the myelin sheath. We described that Rac1 GTP ase regulates actin polymerization in SLI after injury. It has been previously reported that Rac-dependent cytoskeletal reorganization also plays an important role in myelination during the development of peripheral nerves. Thus, our findings suggest that Rac-dependent actin polymerization controls both myelination and demyelination in the peripheral nerves. We further discuss our new findings in relation to Schwann cell dedifferentiation and segmental demyelination.

摘要

周围神经损伤后,华勒氏变性始于髓鞘沿施密特-兰特曼切迹(SLI)处发生典型的碎片化,形成髓鞘卵圆体。这种脱髓鞘过程需要施万细胞的细胞骨架结构发生显著变化。我们最近发现,SLI周围的肌动蛋白聚合是髓鞘裂解的重要步骤。我们描述了Rac1 GTP酶在损伤后调节SLI处的肌动蛋白聚合。此前有报道称,Rac依赖的细胞骨架重组在周围神经发育过程中的髓鞘形成中也起重要作用。因此,我们的研究结果表明,Rac依赖的肌动蛋白聚合控制着周围神经的髓鞘形成和脱髓鞘过程。我们进一步讨论了与施万细胞去分化和节段性脱髓鞘相关的新发现。

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Rac1 GTPase controls myelination and demyelination.Rac1 GTP酶控制髓鞘形成和脱髓鞘过程。
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Wallerian demyelination: chronicle of a cellular cataclysm.华勒氏变性:一场细胞灾难的编年史。
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