School of Life Sciences, Shanghai University, Shanghai, 200444, China.
Department of Neurology, Changzheng Hospital, Shanghai, 200003, China.
Neurochem Res. 2017 Oct;42(10):2933-2939. doi: 10.1007/s11064-017-2324-7. Epub 2017 Jun 16.
Oligodendrocyte precursor cell (OPC) development into myelinated oligodendrocytes demands vigorous membrane addition. Since myristoylated alanine-rich C-kinase substrate (MARCKS) reportedly contributes to Ras-associated protein (Rab)-10-associated vesicle insertion into neuronal membranes, we investigated the role of MARCKS in OPC maturation. We found that either knockdown of MARCKS or interruption of its interaction with Rab10 would cause a decrease of the cell membrane area during OPC development. Enhanced MARCKS phosphorylation by Nogo66 or myelin debris treatment inhibited OPC maturation, while its dephosphorylation by protein phosphatase 2 A activator D-erythro-sphingosine promoted OPC development in the presence of myelin debris. Our results demonstrated that MARCKS is involved in OPC maturation by interacting with Rab10.
少突胶质前体细胞（OPC）向有髓鞘的少突胶质细胞的分化需要大量的膜添加。因为据报道肉豆蔻酰化丙氨酸丰富的 C 激酶底物（MARCKS）有助于 Ras 相关蛋白（Rab）-10 相关囊泡插入神经元膜，我们研究了 MARCKS 在 OPC 成熟中的作用。我们发现，MARCKS 的敲低或与 Rab10 的相互作用中断都会导致 OPC 发育过程中细胞膜面积的减少。Nogo66 或髓鞘碎片处理增强 MARCKS 的磷酸化会抑制 OPC 的成熟，而蛋白磷酸酶 2A 激活剂 D-erythro-sphingosine 使其去磷酸化则会在髓鞘碎片存在的情况下促进 OPC 的发育。我们的结果表明，MARCKS 通过与 Rab10 相互作用参与 OPC 的成熟。
