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脑源性神经营养因子在体外分化过程中诱导小鼠成年海马前体细胞的存活和迁移。

Brain-Derived Neurotrophic Factor Induces Cell Survival and the Migration of Murine Adult Hippocampal Precursor Cells During Differentiation In Vitro.

作者信息

Ortiz-López Leonardo, Vega-Rivera Nelly Maritza, Babu Harish, Ramírez-Rodríguez Gerardo Bernabé

机构信息

Laboratory of Neurogenesis, Division of Clinical Investigations, National Institute of Psychiatry "Ramón de la Fuente Muñiz", Calzada México-Xochimilco No. 101, Colonia San Lorenzo Huipulco, Delegación Tlalpan, C.P. 14370, Mexico City, Mexico.

Laboratory of Neuropsychopharmacology, Division of Neurosciences, National Institute of Psychiatry "Ramón de la Fuente Muñiz", Calz. México-Xochimilco 101, 14370, Mexico City, Mexico.

出版信息

Neurotox Res. 2017 Jan;31(1):122-135. doi: 10.1007/s12640-016-9673-x. Epub 2016 Sep 24.

Abstract

The generation of new neurons during adulthood involves local precursor cell migration and terminal differentiation in the dentate gyrus. These events are influenced by the hippocampal microenvironment. Brain-derived neurotrophic factor (BDNF) is relevant for hippocampal neuronal development and behavior. Interestingly, studies that have been performed in controlled in vitro systems that involve isolated precursor cells that were derived from the dentate gyrus (AHPCs) have shown that BDNF induces the activation of the TrkB receptor and, consequentially, might activate signaling pathways that favor survival and neuronal differentiation. Based on the fact that the cellular events of AHPCs that are induced by single factors can be studied in this controlled in vitro system, we investigated the ability of BDNF and the involvement of protein kinase C (PKC), as one of the TrkB-downstream activated signaling proteins, in the regulation of migration, here reflected by motility, of AHPCs. Precursor cells were cultured following a concentration-response curve (1-640 ng/ml) for 24 or 96 h. We found that BDNF favored cell survival without altering the viability under culture proliferative conditions of the AHPCs. Concomitantly, glial- and neuronal-differentiated precursor cells increased as a consequence of survival promoted by BDNF. Additionally, pharmacological approaches showed that BDNF (40 ng/ml)-induced migration of AHPCs was blocked with the compounds K252a and GF109203x, which prevent the activation of TrkB and PKC, respectively. The results indicate that in the in vitro migration of differentiated AHPCs it is involved the BDNF and TrkB cascade. Our results provide additional information about the mechanism by which BDNF impacts adult neurogenesis in the hippocampus.

摘要

成年期新神经元的生成涉及齿状回中局部前体细胞的迁移和终末分化。这些事件受海马微环境的影响。脑源性神经营养因子(BDNF)与海马神经元发育及行为相关。有趣的是,在涉及源自齿状回的分离前体细胞(AHPCs)的体外对照系统中进行的研究表明,BDNF可诱导TrkB受体激活,进而可能激活有利于存活和神经元分化的信号通路。基于在这种体外对照系统中可以研究单一因子诱导的AHPCs细胞事件这一事实,我们研究了BDNF的作用以及蛋白激酶C(PKC)作为TrkB下游激活的信号蛋白之一在AHPCs迁移调节中的作用,此处迁移以运动性来反映。前体细胞按照浓度 - 反应曲线(1 - 640 ng/ml)培养24或96小时。我们发现BDNF有利于细胞存活,而不改变AHPCs在培养增殖条件下的活力。同时,由于BDNF促进存活,胶质细胞和神经元分化的前体细胞数量增加。此外,药理学方法表明,BDNF(40 ng/ml)诱导的AHPCs迁移被化合物K252a和GF109203x阻断,这两种化合物分别可阻止TrkB和PKC的激活。结果表明,在分化的AHPCs的体外迁移过程中,BDNF和TrkB级联反应参与其中。我们的结果为BDNF影响海马体成年神经发生的机制提供了更多信息。

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