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脂磷壁酸诱导的局灶性脱髓鞘后延髓中少突胶质前体细胞依赖 VEGF 和 PDGF 的增殖。

VEGF- and PDGF-dependent proliferation of oligodendrocyte progenitor cells in the medulla oblongata after LPC-induced focal demyelination.

机构信息

Department of Applied Biology, Kyoto Institute of Technology, Matsugasaki, Sakyo-ku, Kyoto 606-8585, Japan.

Department of Biology, Graduate School of Science, Kobe University, Kobe, 657-8501, Japan.

出版信息

J Neuroimmunol. 2019 Jul 15;332:176-186. doi: 10.1016/j.jneuroim.2019.04.016. Epub 2019 Apr 30.

DOI:10.1016/j.jneuroim.2019.04.016
PMID:31075641
Abstract

The myelin sheath is critical in maintaining normal functions of the adult central nervous system (CNS) and the loss of the myelin sheath results in various neurological diseases. Although remyelination is the intrinsic repair system against demyelination that new myelin sheath is formed around axons in the adult CNS, little has been reported on remyelination system in the medulla oblongata. In the present study, we showed that the proliferation of oligodendrocyte progenitor cells (OPCs) was increased in the medulla oblongata by lysophosphatidylcholine (LPC)-induced focal demyelination, but that of NSCs was not changed. The inhibition of vascular endothelial growth factor (VEGF)- and platelet-derived growth factor (PDGF)-signaling suppressed the proliferation of OPCs by LPC-induced demyelination. Thus, the present study indicates that resident OPCs contribute to focal remyelination and VEGF and PDGF signaling is required for the proliferation of OPCs in the medulla oblongata of the adult mouse.

摘要

髓鞘对于维持成年中枢神经系统(CNS)的正常功能至关重要,而髓鞘的丧失会导致各种神经疾病。尽管髓鞘的再形成是针对脱髓鞘的固有修复系统,即在成年 CNS 中的轴突周围形成新的髓鞘,但关于延髓中的髓鞘再形成系统的报道却很少。在本研究中,我们发现溶血性磷脂酰胆碱(LPC)诱导的局灶性脱髓鞘可增加延髓中少突胶质前体细胞(OPC)的增殖,但神经干细胞(NSC)的增殖并未改变。血管内皮生长因子(VEGF)和血小板衍生生长因子(PDGF)信号的抑制可抑制 LPC 诱导的脱髓鞘后 OPC 的增殖。因此,本研究表明,固有 OPC 有助于局灶性髓鞘再形成,而 VEGF 和 PDGF 信号对于成年小鼠延髓中 OPC 的增殖是必需的。

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