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SVCT2 由小脑前体细胞表达,这些细胞在抗坏血酸的作用下分化为神经元。

SVCT2 Is Expressed by Cerebellar Precursor Cells, Which Differentiate into Neurons in Response to Ascorbic Acid.

机构信息

Centro de Microscopía Avanzada CMA-BIOBIO, Departamento de Biología Celular, Laboratorio de Neurobiología y Células Madres, Facultad de Ciencias Biológicas, Universidad de Concepción, Concepción, Chile.

出版信息

Mol Neurobiol. 2018 Feb;55(2):1136-1149. doi: 10.1007/s12035-016-0366-5. Epub 2017 Jan 17.

DOI:10.1007/s12035-016-0366-5
PMID:28097475
Abstract

Ascorbic acid (AA) is a known antioxidant that participates in a wide range of processes, including stem cell differentiation. It enters the cell through the sodium-ascorbate co-transporter SVCT2, which is mainly expressed by neurons in the adult brain. Here, we have characterized SVCT2 expression in the postnatal cerebellum in situ, a model used for studying neurogenesis, and have identified its expression in granular precursor cells and mature neurons. We have also detected SVCT2 expression in the cerebellar cell line C17.2 and in postnatal cerebellum-derived neurospheres in vitro and have identified a tight relationship between SVCT2 expression and that of the stem cell-like marker nestin. AA supplementation potentiates the neuronal phenotype in cerebellar neural stem cells by increasing the expression of the neuronal marker β III tubulin. Stable over-expression of SVCT2 in C17.2 cells enhances β III tubulin expression, but it also increases cell death, suggesting that AA transporter levels must be finely tuned during neural stem cell differentiation.

摘要

抗坏血酸(AA)是一种已知的抗氧化剂,参与广泛的过程,包括干细胞分化。它通过钠-抗坏血酸盐协同转运蛋白 SVCT2 进入细胞,SVCT2 主要由成年大脑中的神经元表达。在这里,我们对出生后小脑的 SVCT2 表达进行了原位研究,小脑是用于研究神经发生的模型,并在颗粒前体细胞和成熟神经元中鉴定出了其表达。我们还在小脑细胞系 C17.2 和体外培养的出生后小脑源性神经球中检测到了 SVCT2 的表达,并发现 SVCT2 的表达与干细胞样标志物巢蛋白之间存在紧密关系。AA 补充通过增加神经元标志物 β III 微管蛋白的表达来增强小脑神经干细胞的神经元表型。C17.2 细胞中 SVCT2 的稳定过表达增强了 β III 微管蛋白的表达,但也增加了细胞死亡,这表明在神经干细胞分化过程中,AA 转运体水平必须精细调节。

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Mol Neurobiol. 2017 Sep;54(7):5449-5467. doi: 10.1007/s12035-016-0081-2. Epub 2016 Sep 5.
2
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Unconventional Neurogenic Niches and Neurogenesis Modulation by Vitamins.
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