gp130信号参与了神经前体细胞(NPC)的自我更新,敲除gp130分子的胚胎不能正常地发育,可导致胎儿在出生前夭折。CXCR4是趋化因子基质细胞源因子(stromalcellderivedfactor-1α,SDF-1α)已知的唯一受体,表达CXCR4的NPC可在体外被SDF-1α趋化而定向迁移,在神经功能缺损的修复中起着重要的作用。gp130和CXCR4分子之间可能存在着一定的相关性。本实验在发现NPC表达gp130和CXCR4的基础上,采用gp130激发型单克隆抗体激发NPC,结果表明能上调NPC表达CXCR4分子以及增强NPC的迁徙能力,从而揭示了gp130信号在胚胎NPC定向迁移中可能起着重要的作用。 The gp130 signal is involved in the self-renewal of neural precursor cells (NPCs), and embryos that knock out gp130 molecules do not develop normally, resulting in the prenatal loss of the fetus. CXCR4 is the only known receptor for stromal cell-derived factor-1α (SDF-1α). CXCR4-expressing NPCs can be targeted to migrate in vitro by SDF-1α chemotaxis and play a role in the repair of neurological deficits Important role. There may be some correlation between gp130 and CXCR4 molecules. In the present study, gp130-induced monoclonal antibody was used to stimulate NPC based on the results of gp130 and CXCR4 expression in NPC. The results showed that up-regulating the expression of CXCR4 in NPC and enhancing the migratory ability of NPC could reveal the possible role of gp130 in the directional migration of NPC It plays an important role.