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Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation

Directed migration of the transplanted mesenchymal stem cells (MSCs) to the lesion sites plays a pivotal role in the efficacy of cell-based therapy. Our previous study demonstrates that MSCs under varying neural differentiation states possess different migratory capacities in response to chemoattrac...

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Autores principales: Hu, Ya’nan, Lu, Junhou, Xu, Xiaojing, Lyu, Jingya, Zhang, Huanxiang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5577153/
https://www.ncbi.nlm.nih.gov/pubmed/28855566
http://dx.doi.org/10.1038/s41598-017-09736-7
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author Hu, Ya’nan
Lu, Junhou
Xu, Xiaojing
Lyu, Jingya
Zhang, Huanxiang
author_facet Hu, Ya’nan
Lu, Junhou
Xu, Xiaojing
Lyu, Jingya
Zhang, Huanxiang
author_sort Hu, Ya’nan
collection PubMed
description Directed migration of the transplanted mesenchymal stem cells (MSCs) to the lesion sites plays a pivotal role in the efficacy of cell-based therapy. Our previous study demonstrates that MSCs under varying neural differentiation states possess different migratory capacities in response to chemoattractants. However, the underlying mechanism has not been fully addressed. Herein, we show that the assembly and turnover of focal adhesions, the phosphorylation of FAK and paxillin, and the reorganisation of F-actin in MSCs are closely related to their differentiation states in response to SDF-1α. Upon SDF-1α stimulation, FAs turnover more rapidly with the most obvious reduction in the existing time of FAs in MSCs of 24-h preinduction that exhibit the most effective migration towards SDF-1α. Further, we confirm that PI3K/Akt and MAPK pathways participate in the regulation of SDF-1α-induced cell migration and FA assembly, and moreover, that the regulatory effects vary greatly depending on the differentiation states. Collectively, these results demonstrate that FA assembly and turnover, which is accompanied with F-actin reorganisation in response to SDF-1α, correlates closely with the differentiation states of MSCs, which might contribute to the different chemotactic responses of these cells, and thus help develop new strategy to improve the efficacy of MSCs-based therapy.
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spelling pubmed-55771532017-09-01 Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation Hu, Ya’nan Lu, Junhou Xu, Xiaojing Lyu, Jingya Zhang, Huanxiang Sci Rep Article Directed migration of the transplanted mesenchymal stem cells (MSCs) to the lesion sites plays a pivotal role in the efficacy of cell-based therapy. Our previous study demonstrates that MSCs under varying neural differentiation states possess different migratory capacities in response to chemoattractants. However, the underlying mechanism has not been fully addressed. Herein, we show that the assembly and turnover of focal adhesions, the phosphorylation of FAK and paxillin, and the reorganisation of F-actin in MSCs are closely related to their differentiation states in response to SDF-1α. Upon SDF-1α stimulation, FAs turnover more rapidly with the most obvious reduction in the existing time of FAs in MSCs of 24-h preinduction that exhibit the most effective migration towards SDF-1α. Further, we confirm that PI3K/Akt and MAPK pathways participate in the regulation of SDF-1α-induced cell migration and FA assembly, and moreover, that the regulatory effects vary greatly depending on the differentiation states. Collectively, these results demonstrate that FA assembly and turnover, which is accompanied with F-actin reorganisation in response to SDF-1α, correlates closely with the differentiation states of MSCs, which might contribute to the different chemotactic responses of these cells, and thus help develop new strategy to improve the efficacy of MSCs-based therapy. Nature Publishing Group UK 2017-08-30 /pmc/articles/PMC5577153/ /pubmed/28855566 http://dx.doi.org/10.1038/s41598-017-09736-7 Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Hu, Ya’nan
Lu, Junhou
Xu, Xiaojing
Lyu, Jingya
Zhang, Huanxiang
Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation
title Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation
title_full Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation
title_fullStr Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation
title_full_unstemmed Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation
title_short Regulation of focal adhesion turnover in SDF-1α-stimulated migration of mesenchymal stem cells in neural differentiation
title_sort regulation of focal adhesion turnover in sdf-1α-stimulated migration of mesenchymal stem cells in neural differentiation
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5577153/
https://www.ncbi.nlm.nih.gov/pubmed/28855566
http://dx.doi.org/10.1038/s41598-017-09736-7
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