AMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury

Abstract It was reported that CXCR4 signaling played an important role in the migration and differentiation of endogenous neural stem cells after spinal cord injury (SCI). However, the molecular mechanism of it is still unclear. Here, we established a model of SCI in rats and AMD3100 was used to tre...

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Autores principales:	Jia-Ming Liu, Kai Zhao, Liu-Xue Du, Yang Zhou, Xin-Hua Long, Xuan-Yin Chen, Zhi-Li Liu
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/4dde248394154018855f2377b83710ff
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spelling	oai:doaj.org-article:4dde248394154018855f2377b83710ff2021-12-02T12:32:51ZAMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury10.1038/s41598-017-00141-82045-2322https://doaj.org/article/4dde248394154018855f2377b83710ff2017-03-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-00141-8https://doaj.org/toc/2045-2322Abstract It was reported that CXCR4 signaling played an important role in the migration and differentiation of endogenous neural stem cells after spinal cord injury (SCI). However, the molecular mechanism of it is still unclear. Here, we established a model of SCI in rats and AMD3100 was used to treat them. The rats were then sacrificed and the injured spinal cord specimens were harvested. Additionally, the neural stem cells (NSCs) line was culture and treated with AMD3100 in vitro. Results showed the locomotor function of SCI rats was worse after treated with AMD3100. And the expression levels of Nestion in neural stem cells and β-tubulin in neuron cells were significantly increased in the injured spinal cord, which can be inhibited by the CXCR4 antagonist of AMD3100. Additionally, the expression of β-catenin and phosphorylase β-catenin protein was significantly down regulated by AMD3100. In vitro, the NSCs proliferation ability was inhibited and the migration was decreased after treated with AMD3100. Also, the expression of Nestion, β-tubulin, β-catenin and phosphorylase β-catenin protein was significantly decreased in AMD3100 group comparing with untreated group. Taken together, this study suggested that AMD3100 could inhibit the migration and differentiation of endogenous neural stem cells in rats with SCI. The mechanism of it maybe that AMD3100 could down regulate of SDF-1/CXCR4 by targeting β-catenin signaling pathway.Jia-Ming LiuKai ZhaoLiu-Xue DuYang ZhouXin-Hua LongXuan-Yin ChenZhi-Li LiuNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-9 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jia-Ming Liu Kai Zhao Liu-Xue Du Yang Zhou Xin-Hua Long Xuan-Yin Chen Zhi-Li Liu AMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury
description	Abstract It was reported that CXCR4 signaling played an important role in the migration and differentiation of endogenous neural stem cells after spinal cord injury (SCI). However, the molecular mechanism of it is still unclear. Here, we established a model of SCI in rats and AMD3100 was used to treat them. The rats were then sacrificed and the injured spinal cord specimens were harvested. Additionally, the neural stem cells (NSCs) line was culture and treated with AMD3100 in vitro. Results showed the locomotor function of SCI rats was worse after treated with AMD3100. And the expression levels of Nestion in neural stem cells and β-tubulin in neuron cells were significantly increased in the injured spinal cord, which can be inhibited by the CXCR4 antagonist of AMD3100. Additionally, the expression of β-catenin and phosphorylase β-catenin protein was significantly down regulated by AMD3100. In vitro, the NSCs proliferation ability was inhibited and the migration was decreased after treated with AMD3100. Also, the expression of Nestion, β-tubulin, β-catenin and phosphorylase β-catenin protein was significantly decreased in AMD3100 group comparing with untreated group. Taken together, this study suggested that AMD3100 could inhibit the migration and differentiation of endogenous neural stem cells in rats with SCI. The mechanism of it maybe that AMD3100 could down regulate of SDF-1/CXCR4 by targeting β-catenin signaling pathway.
format	article
author	Jia-Ming Liu Kai Zhao Liu-Xue Du Yang Zhou Xin-Hua Long Xuan-Yin Chen Zhi-Li Liu
author_facet	Jia-Ming Liu Kai Zhao Liu-Xue Du Yang Zhou Xin-Hua Long Xuan-Yin Chen Zhi-Li Liu
author_sort	Jia-Ming Liu
title	AMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury
title_short	AMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury
title_full	AMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury
title_fullStr	AMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury
title_full_unstemmed	AMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury
title_sort	amd3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/4dde248394154018855f2377b83710ff
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_version_	1718393916973121536

AMD3100 inhibits the migration and differentiation of neural stem cells after spinal cord injury

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