4.6 Article

ProBDNF inhibits collective migration and chemotaxis of rat Schwann cells

期刊

TISSUE & CELL
卷 48, 期 5, 页码 503-510

出版社

CHURCHILL LIVINGSTONE
DOI: 10.1016/j.tice.2016.07.002

关键词

Schwann cell; Neurotrophin; Collective cell migration; Chemotaxis; Nerve development; Nerve regeneration

资金

  1. Sichuan Province Science and Technology Support Program [2013SZ0069]
  2. Sichuan Province Applied Basic Research Program [2010JY0057]
  3. Sichuan Province Development and Regeneration Key Laboratory Program [SYS13-001]
  4. Scientific Research Foundation for the Young Scholars, Sichuan University [2014SCU11 041]

向作者/读者索取更多资源

Schwann cell migration, including collective migration and chemotaxis, is essential for the formation of coordinate interactions between Schwann cells and axons during peripheral nerve development and regeneration. Moreover, limited migration of Schwann cells imposed a serious obstacle on Schwann cell-astrocytes intermingling and spinal cord repair after Schwann cell transplantation into injured spinal cords. Recent studies have shown that mature brain-derived neurotrophic factor, a member of the neurotrophin family, inhibits Schwann cell migration. The precursor form of brain-derived neurotrophic factor, proBDNF, was expressed in the developing or degenerating peripheral nerves and the injured spinal cords. Since the yin and yang of neurotrophin action has been established as a common sense, proBDNF would be expected to promote Schwann cell migration. However, we found, in the present study, that exogenous proBDNF also inhibited in vitro collective migration and chemotaxis of RSC 96 cells, a spontaneously immortalized rat Schwann cell line. Moreover, proBDNF suppressed adhesion and spreading of those cells. At molecular level, proBDNF inhibits F-actin polymerization and focal adhesion dynamics in cultured RSC 96 cells. Therefore, our results suggested a special case against the classical opinion of the yin and yang of neurotrophin action and implied that proBDNF might modulate peripheral nerve development or regeneration and spinal cord repair through perturbing native or transplanted Schwann cell migration. (C) 2016 Elsevier Ltd. All rights reserved.

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