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VEGF treatment promotes bone marrow-derived CXCR4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells

Stem/progenitor cells serve an important role in the process of blood vessel repair. However, the mechanism of vascular repair mediated by C-X-C chemokine receptor type 4-positive (CXCR4(+)) bone marrow-derived mesenchymal stem cells (BMSCs) following myocardial infarction remains unclear. The aim o...

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Autores principales: Li, Qiming, Xia, Shudong, Fang, Hanyun, Pan, Jiansheng, Jia, Yinfeng, Deng, Gang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348687/
https://www.ncbi.nlm.nih.gov/pubmed/28352314
http://dx.doi.org/10.3892/etm.2017.4019
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author Li, Qiming
Xia, Shudong
Fang, Hanyun
Pan, Jiansheng
Jia, Yinfeng
Deng, Gang
author_facet Li, Qiming
Xia, Shudong
Fang, Hanyun
Pan, Jiansheng
Jia, Yinfeng
Deng, Gang
author_sort Li, Qiming
collection PubMed
description Stem/progenitor cells serve an important role in the process of blood vessel repair. However, the mechanism of vascular repair mediated by C-X-C chemokine receptor type 4-positive (CXCR4(+)) bone marrow-derived mesenchymal stem cells (BMSCs) following myocardial infarction remains unclear. The aim of the present study was to investigate the effects of vascular endothelial growth factor (VEGF) on vessel endothelial differentiation from BMSCs. CXCR4(+) BMSCs were isolated from the femoral bone marrow of 2-month-old mice and the cells were treated with VEGF. Expression of endothelial cell markers and the functional properties were assessed by reverse transcription-quantitative polymerase chain reaction, flow cytometry and vascular formation analyses. The results indicated that the CXCR4(+) BMSCs from femoral bone marrow cells expressed putative cell surface markers of mesenchymal stem cells. Treatment with VEGF induced platelet/endothelial cell adhesion molecule-1 (PECAM-1) and von Willebrand factor (vWF) expression at the transcriptional and translational levels, compared with untreated controls. Moreover, VEGF treatment induced CXCR4(+) BMSCs to form hollow tube-like structures on Matrigel, suggesting that the differentiated endothelial cells had the functional properties of blood vessels. The results demonstrate that the CXCR4(+) BMSCs were able to differentiate into vessel endothelial cells following VEGF treatment. For cell transplantation in vascular disease, it may be concluded that CXCR4(+) BMSCs are a novel source of endothelial progenitor cells with high potential for application in vascular repair.
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spelling pubmed-53486872017-03-28 VEGF treatment promotes bone marrow-derived CXCR4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells Li, Qiming Xia, Shudong Fang, Hanyun Pan, Jiansheng Jia, Yinfeng Deng, Gang Exp Ther Med Articles Stem/progenitor cells serve an important role in the process of blood vessel repair. However, the mechanism of vascular repair mediated by C-X-C chemokine receptor type 4-positive (CXCR4(+)) bone marrow-derived mesenchymal stem cells (BMSCs) following myocardial infarction remains unclear. The aim of the present study was to investigate the effects of vascular endothelial growth factor (VEGF) on vessel endothelial differentiation from BMSCs. CXCR4(+) BMSCs were isolated from the femoral bone marrow of 2-month-old mice and the cells were treated with VEGF. Expression of endothelial cell markers and the functional properties were assessed by reverse transcription-quantitative polymerase chain reaction, flow cytometry and vascular formation analyses. The results indicated that the CXCR4(+) BMSCs from femoral bone marrow cells expressed putative cell surface markers of mesenchymal stem cells. Treatment with VEGF induced platelet/endothelial cell adhesion molecule-1 (PECAM-1) and von Willebrand factor (vWF) expression at the transcriptional and translational levels, compared with untreated controls. Moreover, VEGF treatment induced CXCR4(+) BMSCs to form hollow tube-like structures on Matrigel, suggesting that the differentiated endothelial cells had the functional properties of blood vessels. The results demonstrate that the CXCR4(+) BMSCs were able to differentiate into vessel endothelial cells following VEGF treatment. For cell transplantation in vascular disease, it may be concluded that CXCR4(+) BMSCs are a novel source of endothelial progenitor cells with high potential for application in vascular repair. D.A. Spandidos 2017-02 2017-01-02 /pmc/articles/PMC5348687/ /pubmed/28352314 http://dx.doi.org/10.3892/etm.2017.4019 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.
spellingShingle Articles
Li, Qiming
Xia, Shudong
Fang, Hanyun
Pan, Jiansheng
Jia, Yinfeng
Deng, Gang
VEGF treatment promotes bone marrow-derived CXCR4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells
title VEGF treatment promotes bone marrow-derived CXCR4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells
title_full VEGF treatment promotes bone marrow-derived CXCR4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells
title_fullStr VEGF treatment promotes bone marrow-derived CXCR4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells
title_full_unstemmed VEGF treatment promotes bone marrow-derived CXCR4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells
title_short VEGF treatment promotes bone marrow-derived CXCR4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells
title_sort vegf treatment promotes bone marrow-derived cxcr4(+) mesenchymal stromal stem cell differentiation into vessel endothelial cells
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5348687/
https://www.ncbi.nlm.nih.gov/pubmed/28352314
http://dx.doi.org/10.3892/etm.2017.4019
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