Rho激酶通过钙依赖的细胞骨架调节来调控海马神经元的轴突生长。
Rho kinase regulates neurite outgrowth of hippocampal neurons via calcium dependent cytoskeleton regulation.
作者信息
Ji Zhisheng, Cai Zhenbin, Zhang Jifeng, Liu Nannuan, Chen Jing, Tan Minghui, Lin Hongsheng, Guo Guoqing
机构信息
Department of Orthopedics, The First Affiliated Hospital of Jinan UniversityGuangzhou 510630, China; Department of Anatomy, Medical College of Jinan UniversityGuangzhou 510630, China.
Department of Orthopedics, The First Affiliated Hospital of Jinan University Guangzhou 510630, China.
出版信息
Am J Transl Res. 2017 Feb 15;9(2):762-773. eCollection 2017.
OBJECTIVE
To investigate whether calcium is involved in downstream signal transduction in neurite outgrowth regulated by Rho kinase.
METHODS
primary hippocampal neurons were cultured and treated with Rho kinase agonist (LPA) or antagonist (Y-27632). Then, the cytoskeleton and neurite outgrowth were observed. After addition of calcium antagonist BAPTA/AM to reduce intracellular calcium, the cytoskeleton distribution and neurite outgrowth were observed.
RESULTS
The activation or inhibition of Rho kinase could significantly alter the number and length of neurites of hippocampal neurons. Rho kinase regulated the cytoskeleton to regulate the neurite outgrowth, and LPA could significantly increase intracellular calcium. After BAPTA/AM treatment, the length and branch number of neurites of neurons reduced markedly. BAPTA/AM was able to reduce intracellular calcium and decrease neuronal cytoskeleton. Treatment with both BAPTA/AM and LPA could stop the retraction of neurites, but the length and branch number of neurites remained unchanged after treatment with Y-27632 and LPA.
CONCLUSION
Calcium may affect the cytoskeleton arrangement to regulate neurite outgrowth, and calcium is involved in the downstream signal transduction of Rho kinase regulated neurite outgrowth of hippocampal neurons.
目的
研究钙是否参与Rho激酶调节的神经突生长的下游信号转导。
方法
培养原代海马神经元，并用Rho激酶激动剂（LPA）或拮抗剂（Y-27632）处理。然后，观察细胞骨架和神经突生长情况。加入钙拮抗剂BAPTA/AM以降低细胞内钙后，观察细胞骨架分布和神经突生长情况。
结果
Rho激酶的激活或抑制可显著改变海马神经元神经突的数量和长度。Rho激酶通过调节细胞骨架来调节神经突生长，LPA可显著增加细胞内钙。BAPTA/AM处理后，神经元神经突的长度和分支数明显减少。BAPTA/AM能够降低细胞内钙并减少神经元细胞骨架。BAPTA/AM和LPA共同处理可阻止神经突回缩，但Y-27632和LPA处理后神经突的长度和分支数保持不变。
结论
钙可能通过影响细胞骨架排列来调节神经突生长，且钙参与Rho激酶调节海马神经元神经突生长的下游信号转导。
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