Mechanism of neurite outgrowth through chloride ion dependent regulation of G protein signaling

在大鼠嗜铬细胞瘤PC12D细胞中，NGF诱导的突起生长在低氯条件下受到抑制。在亲代PC12细胞中，神经生长因子诱导的突起生长也被低氯离子条件下抑制。然而，在PC12细胞中，Y-27632处理并不能挽救低氯条件下抑制突起生长的作用。PC12D细胞的RhoA蛋白表达水平高于PC12细胞。这些观察结果提示，两种细胞中蛋白质表达水平的差异可能导致对Rho激酶抑制剂的不同敏感性。

In rat pheochromocytoma PC12D cells, NGF-induced neurite outgrowth was inhibited in low Cl^-condition. This inhibition was partially rescued by the treatment of cells with Rho kinase inhibitor Y-27632.In parental PC12 cells, NGF-induced neurite outgrowth was also inhibited by in low Cl^-condition. However, in PC12 cells, inhibition of neurite outgrowth in the low Cl^-condition was not rescued by Y-27632 treatment. The protein expression level of RhoA in PC12D cells was higher than that in PC12 cells. These observations suggest that difference of protein expression level in both cells might cause different sensitivity to Rho kinase inhibitor.