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首页> 外文期刊>Journal of Cellular Physiology >The induction of tuftelin expression in PC12 cell line during hypoxia and NGF-induced differentiation.
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The induction of tuftelin expression in PC12 cell line during hypoxia and NGF-induced differentiation.

机译：tuftelin表达的诱导PC12细胞在缺氧和NGF-induced线分化。

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摘要

The tuftelin protein isoforms undergo post-translation modifications, and are ubiquitously expressed in various tissues in embryos, adults, and tumors. Developmental and pathological studies suggested an apparent correlation between oxygen deprivation and tuftelin expression. The aim of the study was therefore to investigate the effect of a pathological insult (hypoxia) and a physiological growth factor (NGF), which antagonistically regulate HIF1 expression, on tuftelin expression using the neuronal PC12 cell model. In the present study, we first demonstrated the expression of tuftelin in PC12 cells, providing an experimental system to investigate the pathophysiological role of tuftelin. Furthermore, we demonstrated the induction of tuftelin during hypoxia by oxygen deprivation and during chemical hypoxia by cobalt chloride. Down-regulation of HIF1alpha mRNA blocked hypoxia-induced HIF1alpha expression, and reduced by 89% hypoxia-induced tuftelin expression. In mice, intraperitoneal injection of cobalt chloride significantly induced tuftelin mRNA and protein expression in the brain. During NGF-mediated PC12 differentiation, tuftelin expression was significantly induced in correlation with neurite outgrowth. This induction was partially blocked by K252a, a selective antagonist of the NGF receptor TrkA, indicating the involvement of the TrkA-signaling pathways in tuftelin induction by NGF. Revealing the physiological role of tuftelin will clarify mechanisms related to the "hypoxic genome," and NGF-induced neurotrophic and angiogenic effects.
机译：tuftelin蛋白亚型进行译后修改,在各种组织中广泛表达胚胎、成人和肿瘤。病理研究表明一个明显缺氧和之间的相关性tuftelin表达式。因此,调查的影响(缺氧)和生理病理侮辱生长因子(神经生长因子),反对地调节HIF1的表达,tuftelin表达式使用神经PC12细胞模型。本研究,我们首先证明了表达式的tuftelin PC12细胞,提供一个实验系统研究tuftelin的病理生理作用。我们演示了tuftelin的感应在化学缺氧,缺氧通过氯化钴缺氧。低氧诱导HIF1alpha HIF1alpha mRNA阻塞低氧诱导表达,减少了89%tuftelin表达式。注射氯化钴诱导tuftelin mRNA和蛋白表达大脑。分化,tuftelin表达式与神经突明显诱导相关结果。由选择性K252a神经生长因子的拮抗剂受体TrkA,指示的参与TrkA-signaling通路tuftelin感应神经生长因子。将澄清相关机制“缺氧吗和NGF-induced神经营养基因。血管生成的影响。

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