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Molecular mechanisms that function in oligodendrocyte myelination

Molecular mechanisms that function in oligodendrocyte myelination
少突胶质细胞髓鞘形成的分子机制
批准号:
24890291
负责人:
SHIMIZU Takeshi
金额:
$1.91万
依托单位国家:
日本
项目类别:
Grant-in-Aid for Research Activity Start-up
财政年份:
2012
资助国家:
日本
项目状态:
已结题
起止时间:
2012-08-31 至 2014-03-31

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中文摘要
翻译
少突胶质细胞是中枢神经系统中形成髓鞘的神经轴突的胶质细胞。髓磷脂使轴突隔绝,增加神经元动作电位的传导速度。最近的研究表明,力学因素会影响细胞的各种特性。机械刺激可通过黏附相关机械传感器的构象变化传导到细胞内的生化信号。我们分析了少突胶质细胞形态和髓鞘形成与机械传感器的关系。此外,我们发现非规范Wnt信号在脱髓鞘小鼠模型中上调。我们研究了非典型Wnt信号通路是否在实验性自身免疫性脑脊髓炎诱导的神经病理中起作用。
英文摘要
Oligodendrocytes are glial cells that myelinate neuronal axons in the central nervous system. Myelin insulates axons to increase conduction velocity of neuronal action potentials. Recent studies have shown that mechanical factors influence various cell properties. Mechanical stimulation can be transduced to intracellular biochemical signals through conformational changes in focal adhesion-related mechanosensors. We analyzed oligodendrocyte morphology and myelination in relation with the mechanosensors. In addition, we found that non-canonical Wnt signaling was up-regulated in a demyelinating mouse model. We examined whether non-canonical Wnt signaling pathway had a role in the Experimental Autoimmune Encephalomyelitis-induced neural pathology.
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