中国科技核心期刊
CN:31-1600/Q
ISSN:1004-0374
“健康与疾病的免疫”国际学术研讨会通知      关于有网站冒充本刊网站的声明
《生命科学》 2015, 27(10): 1261-1267
CXCL12/CXCR4轴对NPC调节的研究进展
王 朋1,2,宋淑亮2,3,梁 浩2,3,崔宁珊2,3,崔 超2,3,吉爱国1,2,3*
(1 山东大学药学院,济南 250012;2 山东大学威海国际生物技术研发中心,威海 264209;3 山东大学海洋学院,威海 264209)
摘 要:基质细胞衍生因子1α(SDF-1α/CXCL12) 属于趋化因子CXC 家族,与其受体CXCR4 组成的CXCL12/CXCR4 轴,在大脑生理和病理状态下都发挥着重要作用。 CXCL12 能与神经祖细胞(NPC) 表面上的受体CXCR4 结合,从而激活CXCR4 下游不同的信号通路,参与调节NPC 静息、激活、增殖、迁移和分化等活动。在中枢神经系统(CNS) 疾病发生后,大脑中CXCL12 会激活内源的NPC,促进NPC 增殖并迁移至病灶区域,最终分化为神经元并整合入神经系统,促进神经功能恢复。深入理解CNS疾病时期CXCL12/CXCR4 轴对NPC 调控作用,对内源性和外源性的NPC 应用于CNS 疾病具有重要意义。现主要对CXCL12/CXCR4 轴调控NPC 活动的作用机制及相关信号通路进行综述。
 
Research advances on CXCL12/CXCR4 axis to regulate NPC
WANG Peng1,2, SONG Shu-Liang2,3, LIANG Hao2,3, CUI Ning-Shan2,3, CUI Chao2,3, JI Ai-Guo1,2,3*
(1 School of Pharmaceutical Sciences, Shandong University, Jinan 250012, China; 2 Marine College, Shandong University, Weihai 264209, China; 3 Weihai International Biotechnology Research & Development Centre, Weihai 264209, China)
Abstract: The stromal cell-derived factor 1 alpha (SDF-1α or CXCL12) belongs to the CXC chemokine family, and CXCL12/CXCR4 biological axis plays an important role in brain physiology and pathology. CXCL12 binds to CXCR4, the receptor of CXCL12 on neural progenitor cells (NPC). Then the downstream signaling pathways of CXCR4 will be activated, which can regulate the quiescence, activation, proliferation, migration and differentiation of NPC. After the central nervous system (CNS) disease appears, CXCL12 generated in the brain will activate the
    endogenous NPC, promote the proliferation and migration of NPC to the lesion area. NPC will eventually differentiate into neurons that could integrate into the nervous system to promote nerve function recovery. Deeply understanding the effects of CXCL12/CXCR4 biological axis in regulation of NPC during CNS disease has an important significance for the NPC application in CNS disease. This review summarizes research advances on the mechanism and related signaling pathways of CXCL12/CXCR4 axis in regulation of NPC.
 
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