Wang Tianyi, Yuan Wenqi, Liu Yong, Zhang Yanjun, Wang Zhijie, Zhou Xianhu, Ning Guangzhi, Zhang Liang, Yao Liwei, Feng Shiqing, Kong Xiaohong
Department of Orthopedics, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China ; Department of Orthopedics, The 266th Hospital of the Chinese People's Liberation Army, Chengde, Hebei 067000, P.R. China.
Department of Orthopedics, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China.
Biomed Rep. 2015 Mar;3(2):141-146. doi: 10.3892/br.2014.401. Epub 2014 Dec 11.
Patients with spinal cord injuries can develop severe neurological damage and dysfunction, which is not only induced by primary but also by secondary injuries. As an evolutionarily conserved pathway of eukaryotes, the JAK-STAT pathway is associated with cell growth, survival, development and differentiation; activation of the JAK-STAT pathway has been previously reported in central nervous system injury. The JAK-STAT pathway is directly associated with neurogenesis and glia scar formation in the injury region. Following injury of the axon, the overexpression and activation of STAT3 is exhibited specifically in protecting neurons. To investigate the role of the JAK-STAT pathway in neuroprotection, we summarized the effect of JAK-STAT pathway in the following three sections: Firstly, the modulation of JAK-STAT pathway in proliferation and differentiation of neural stem cells and neural progenitor cells is discussed; secondly, the time-dependent effect of JAK-STAT pathway in reactive astrocytes to reveal their capability of neuroprotection is revealed and lastly, we focus on how the astrocyte-secretory polypeptides (astrocyte-derived cytokines and trophic factors) accomplish neuroprotection via the JAK-STAT pathway.
脊髓损伤患者会出现严重的神经损伤和功能障碍，这不仅由原发性损伤引起，也由继发性损伤导致。作为真核生物进化上保守的途径，JAK-STAT途径与细胞生长、存活、发育和分化相关；先前已有报道JAK-STAT途径在中枢神经系统损伤中被激活。JAK-STAT途径与损伤区域的神经发生和胶质瘢痕形成直接相关。轴突损伤后，STAT3的过表达和激活在保护神经元方面有特异性表现。为了研究JAK-STAT途径在神经保护中的作用，我们在以下三个部分总结了JAK-STAT途径的作用：首先，讨论JAK-STAT途径对神经干细胞和神经祖细胞增殖和分化的调节；其次，揭示JAK-STAT途径在反应性星形胶质细胞中的时间依赖性效应，以显示其神经保护能力；最后，我们关注星形胶质细胞分泌的多肽（星形胶质细胞衍生的细胞因子和营养因子）如何通过JAK-STAT途径实现神经保护。
