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Extracellular zinc and microglial phenotype

机译:细胞外锌和小胶质细胞表型

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Microglia are the resident immune cells of the central nervous system (CNS). When activated by tissue injury or other molecules released from damaged cells following CNS disorders such as brain ischemia and multiple sclerosis (MS), microglia retract their ramifications to form an activated amoeboid morphology. Recent studies have demonstrated that activated microglia can exert either pro-inflammatory or anti-inflammatory properties, which is thought to be regulated by factors in the microenvironment. On the other hand, zinc is concentrated in neurons of specific regions of the central nervous system (CNS) including the hippocampus and spinal cord. Massive amounts of zinc are released by neurons under severe conditions in which microglial activation occurs. This article discusses the role of extracellular zinc in regulation of microglial activation in animal models of brain ischemia and MS, as described in recent literatures by our group and the others. In addition, we review that zinc primes microglia via zinc-induced signaling pathway to enhance production of pro-inflammatory cytokines.
机译:小胶质细胞是中枢神经系统(CNS)的固有免疫细胞。当神经损伤和中枢神经系统疾病(MS)等中枢神经系统疾病后,由于组织损伤或从受损细胞释放的其他分子激活时,小胶质细胞会缩回其分支,形成活化的变形虫形态。最近的研究表明,活化的小胶质细胞可以发挥促炎或抗炎特性,这被认为是由微环境中的因素调节的。另一方面,锌集中在中枢神经系统(CNS)特定区域的神经元中,包括海马和脊髓。在发生小胶质细胞活化的严重条件下,神经元会释放大量的锌。本文讨论了脑缺血和MS动物模型中细胞外锌在调控小胶质细胞活化中的作用,正如我们小组和其他组织在最近的文献中所描述的那样。另外,我们回顾了锌通过锌诱导的信号通路引发小胶质细胞,以增强促炎细胞因子的产生。

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