瘦素通过Wnt信号通路调控PC12细胞中Tau磷酸化

Q1 Medicine
Neurosignals Pub Date : 2016-10-24 DOI:10.1159/000442616
Zijuan Zhang, Meixia Guo, Juan Zhang, C. Du, Y. Xing
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引用次数: 6

摘要

背景/目的:瘦素是一种在大脑内源性产生的脂肪细胞因子,在阿尔茨海默病(AD)中减少,并且在体外和体内也被证明可以降低Aβ水平。一系列证据表明,瘦素可以减少神经细胞和AD转基因小鼠模型中Aβ的产生和tau蛋白的磷酸化。在此,我们研究了瘦素激活的信号通路,以更好地了解其作用机制。方法:采用Western blot检测磷酸化tau蛋白和Bax蛋白的表达水平,RT-PCR检测Bax mRNA的表达水平。结果:Leptin治疗显著减弱了a β-诱发的tau磷酸化和Bax水平,这种作用可以通过Wnt信号拮抗剂逆转。结论:瘦素可能是通过wnt信号通路治疗AD的新途径。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Leptin Regulates Tau Phosphorylation through Wnt Signaling Pathway in PC12 Cells
Background/Aims: Leptin, an adipocytokine produced endogenously in the brain, is decreased in Alzheimer's disease(AD) and has also been shown to reduce Aβ levels in vitro and in vivo. Sets of evidence show that leptin reduces Aβ production and tau phosphorylation in neuronal cells and transgenic mice models of AD. Herein, we investigated the signaling pathway activated by leptin, to better understand its mechanism of action. Methods: Western blotting was performed to assess the levels of phosphor-tau and Bax, RT-PCR to check the mRNA level of Bax. Results: Leptin treatment significantly blunted Aβ-evoked tau phosphorylation and Bax levels, effects of which could be reversed by antagonist of Wnt signaling. Conclusion: The data indicate that Leptin may provide a novel therapeutic approach to AD treatment via wnt signaling.
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来源期刊
Neurosignals
Neurosignals 医学-神经科学
CiteScore
3.40
自引率
0.00%
发文量
3
审稿时长
>12 weeks
期刊介绍: Neurosignals is an international journal dedicated to publishing original articles and reviews in the field of neuronal communication. Novel findings related to signaling molecules, channels and transporters, pathways and networks that are associated with development and function of the nervous system are welcome. The scope of the journal includes genetics, molecular biology, bioinformatics, (patho)physiology, (patho)biochemistry, pharmacology & toxicology, imaging and clinical neurology & psychiatry. Reported observations should significantly advance our understanding of neuronal signaling in health & disease and be presented in a format applicable to an interdisciplinary readership.
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