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Thioredoxin-2 modulates neuronal programmed cell death in the embryonic chick spinal cord in basal and target-deprived conditions.

机译:硫氧还蛋白2调节基础和靶标剥夺条件下胚胎雏鸡脊髓中神经元程序性细胞死亡。

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摘要

Thioredoxin-2 (Trx2) is a mitochondrial protein using a dithiol active site to reduce protein disulfides. In addition to the cytoprotective function of this enzyme, several studies have highlighted the implication of Trx2 in cellular signaling events. In particular, growing evidence points to such roles of redox enzymes in developmental processes taking place in the central nervous system. Here, we investigate the potential implication of Trx2 in embryonic development of chick spinal cord. To this end, we first studied the distribution of the enzyme in this tissue and report strong expression of Trx2 in chick embryo post-mitotic neurons at E4.5 and in motor neurons at E6.5. Using in ovo electroporation, we go on to highlight a cytoprotective effect of Trx2 on the programmed cell death (PCD) of neurons during spinal cord development and in a novel cultured spinal cord explant model. These findings suggest an implication of Trx2 in the modulation of developmental PCD of neurons during embryonic development of the spinal cord, possibly through redox regulation mechanisms.
机译:硫氧还蛋白2(Trx2)是一种线粒体蛋白,利用二硫醇活性位点来减少蛋白二硫键。除了该酶的细胞保护功能外,一些研究还强调了Trx2在细胞信号转导事件中的意义。特别是,越来越多的证据表明氧化还原酶在中枢神经系统中发生的发育过程中的这种作用。在这里,我们调查Trx2在雏鸡脊髓胚胎发育中的潜在影响。为此,我们首先研究了该酶在该组织中的分布,并报告了Trx2在有丝分裂后的神经元E4.5和运动神经元在E6.5的强表达。在卵内电穿孔中,我们继续强调Trx2对脊髓发育过程中和新型培养的脊髓外植体模型中神经元程序性细胞死亡(PCD)的细胞保护作用。这些发现表明,Trx2可能通过氧化还原调节机制在脊髓胚胎发育过程中参与神经元发育PCD的调节。

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