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

在大鼠嗜铬细胞瘤PC 12 D细胞中，在低Cl^-条件下，NGF诱导的神经突起生长受到抑制。Rho激酶抑制剂Y-27632可部分解除这种抑制作用。在亲本PC 12细胞中，在低Cl^-条件下，NGF诱导的神经突起生长也受到抑制。然而，在PC 12细胞中，Y-27632处理不能挽救低Cl^-条件下对神经突生长的抑制。RhoA蛋白在PC 12 D细胞中的表达水平高于PC 12细胞。这些结果表明，在两种细胞中的蛋白表达水平的差异可能导致不同的敏感性Rho激酶抑制剂。

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.