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维生素D对HN9.10e胚胎海马细胞及MPTP诱导的帕金森病小鼠模型海马的影响。

Effect of Vitamin D in HN9.10e Embryonic Hippocampal Cells and in Hippocampus from MPTP-Induced Parkinson's Disease Mouse Model.

作者信息

Cataldi Samuela, Arcuri Cataldo, Hunot Stéphane, Mecca Carmen, Codini Michela, Laurenti Maria E, Ferri Ivana, Loreti Elisabetta, Garcia-Gil Mercedes, Traina Giovanna, Conte Carmela, Ambesi-Impiombato Francesco S, Beccari Tommaso, Curcio Francesco, Albi Elisabetta

机构信息

Department of Pharmaceutical Sciences, University of Perugia, Perugia, Italy.

Department of Experimental Medicine, University of Perugia, Perugia, Italy.

出版信息

Front Cell Neurosci. 2018 Feb 7;12:31. doi: 10.3389/fncel.2018.00031. eCollection 2018.

Abstract

It has long been proven that neurogenesis continues in the adult brains of mammals in the dentatus gyrus of the hippocampus due to the presence of neural stem cells. Although a large number of studies have been carried out to highlight the localization of vitamin D receptor in hippocampus, the expression of vitamin D receptor in neurogenic dentatus gyrus of hippocampus in Parkinson's disease (PD) and the molecular mechanisms triggered by vitamin D underlying the production of differentiated neurons from embryonic cells remain unknown. Thus, we performed a preclinical study by inducing PD in mice with MPTP and showed a reduction of glial fibrillary acidic protein ( in the dentatus gyrus of hippocampus. Then, we performed an study by inducing embryonic hippocampal cell differentiation with vitamin D. Interestingly, vitamin D stimulates the expression of its receptor. Vitamin D receptor is a transcription factor that probably is responsible for the upregulation of microtubule associated protein 2 and neurofilament heavy polypeptide genes. The latter increases heavy neurofilament protein expression, essential for neurofilament growth. Notably N-cadherin, implicated in activity for dendritic outgrowth, is upregulated by vitamin D.

摘要

长期以来,人们已经证实,由于神经干细胞的存在,哺乳动物成年大脑海马齿状回中会持续发生神经发生。尽管已经开展了大量研究以突出维生素D受体在海马体中的定位,但帕金森病(PD)中海马齿状回神经源性区域维生素D受体的表达以及维生素D引发胚胎细胞分化产生分化神经元的分子机制仍不清楚。因此,我们通过用MPTP诱导小鼠患帕金森病进行了一项临床前研究,结果显示海马齿状回中胶质纤维酸性蛋白减少。然后,我们通过用维生素D诱导胚胎海马细胞分化进行了一项研究。有趣的是,维生素D会刺激其受体的表达。维生素D受体是一种转录因子,可能负责上调微管相关蛋白2和神经丝重多肽基因。后者会增加对神经丝生长至关重要的重神经丝蛋白表达。值得注意的是,参与树突生长活动的N-钙黏着蛋白会被维生素D上调。

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