Suppressor of cytokine signalling-2 and epidermal growth factor regulate neurite outgrowth of cortical neurons
Suppressor of cytokine signalling-2 and epidermal growth factor regulate neurite outgrowth of cortical neurons
复制标题
DOI：
10.1111/j.1460-9568.2004.03698.x
复制
发表时间：
2004-11-01
影响因子：
3.4
通讯作者：
Turnley, AM
中科院分区：
文献类型：
--
作者：
Goldshmit, Y;Greenhalgh, CJ;Turnley, AM
调节神经突生长的因素对于确定中枢神经系统的连接很重要。在这里，我们描述了细胞因子信号传导的细胞内调节因子、细胞因子信号传导抑制因子-2 (SOCS2) 和表皮生长因子 (EGF)，两者在神经发育过程中在皮质板中表达，促进皮质神经元的轴突生长。与野生型神经元相比，过度表达 SOCS2 的转基因小鼠衍生的皮层神经元的神经突生长率增加，初级神经突的长度和数量增加。 EGF 在野生型皮质神经元中产生了类似的效果，并进一步增强了 SOCS2 诱导的神经突生长。 SOCS2 和 EGF 诱导神经突生长的机制至少部分重叠，因为 SOCS2 过表达或 EGF 刺激的神经元中 EGF 受体的磷酸化在酪氨酸 (845) 上增加，两种方案中的 Src 结合位点和神经突生长均被 EGF 受体激酶和 Src 激酶抑制剂阻断。
Factors that regulate neurite outgrowth are important in determining the wiring of the central nervous system. Here we describe that the intracellular regulator of cytokine signalling, suppressor of cytokine signalling-2 (SOCS2) and epidermal growth factor (EGF), both of which are expressed in the cortical plate during neural development, promote neurite outgrowth of cortical neurons. Cortical neurons derived from transgenic mice that over-express SOCS2 had an increased rate of neurite outgrowth and an increased length and number of primary neurites compared with wild-type neurons. EGF produced a similar effect in wild-type cortical neurons and further enhanced the SOCS2-induced neurite outgrowth. The mechanism of neurite outgrowth induction by SOCS2 and EGF at least partially overlapped as phosphorylation of the EGF receptor in SOCS2 over-expressing or EGF-stimulated neurons was increased on Tyrosine(845), the Src binding site and neurite outgrowth in both protocols was blocked by inhibitors of the EGF receptor kinase and Src kinase.