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Neuroprotection via RNA-binding protein RBM3 expression is regulated by hypothermia but not by hypoxia in human SK-N-SH neurons

机译:在人SK-N-SH神经元中通过RNA结合蛋白RBM3表达的神经保护作用受体温过低的调节但不受缺氧的调节

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摘要

ObjectiveTherapeutic hypothermia is an established treatment for perinatal asphyxia. Yet, many term infants continue to die or suffer from neurodevelopmental disability. Several experimental studies have demonstrated a beneficial effect of mild-to-moderate hypothermia after hypoxic injury, but the understanding of hypothermia-induced neuroprotection remains incomplete. In general, global protein synthesis is attenuated by hypothermia, but a small group of RNA-binding proteins including the RNA-binding motif 3 (RBM3) is upregulated in response to cooling. The aim of this study was to establish an in vitro model to investigate the effects of hypoxia and hypothermia on neuronal cell survival, as well as to examine the kinetics of concurrent cold-shock protein RBM3 gene expression.
机译:目的低温治疗是围产期窒息的既定治疗方法。然而,许多足月婴儿继续死亡或患有神经发育障碍。几项实验研究表明,低氧损伤后轻度至中度的体温过低的有益作用,但对体温过低引起的神经保护作用的理解仍然不完整。通常,低温会使整体蛋白质合成减弱,但是响应于冷却,包括RNA结合基序3(RBM3)在内的一小部分RNA结合蛋白被上调。这项研究的目的是建立一个体外模型,以研究缺氧和体温过低对神经元细胞存活的影响,并研究并发冷激蛋白RBM3基因表达的动力学。

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