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: National Institute for Physiological Sciences
• 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
• 起止时间: 2012-08-31 至 2014-03-31
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-24890291/
• 关键词: オリゴデンドロサイト; ミエリン; グリア細胞

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.

少突胶质细胞是中枢神经系统中髓鞘神经元轴突的神经胶质细胞。髓鞘隔离轴突以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性质。机械刺激可以通过局部黏附相关的机械传感器的构象变化而转化为细胞内的生化信号。我们分析了少突胶质细胞的形态和髓鞘形成与机械传感器的关系。此外，我们还发现，在脱髓鞘小鼠模型中，非典型的Wnt信号上调。我们研究了非规范的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。