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EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis

Bronchopulmonary dysplasia (BPD) is the most common type of chronic lung disease in infancy; however, there is no effective treatment for it. In the present study, a neonatal mouse BPD model was established by continuous exposure to high oxygen (HO) levels. Mice were divided randomly into 5 groups:...

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Autores principales: Sun, Chao, Zhang, Shanshan, Wang, Jue, Jiang, Wen, Xin, Qian, Chen, Xiaojing, Zhang, Zhaohua, Luan, Yun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6519997/
https://www.ncbi.nlm.nih.gov/pubmed/31035257
http://dx.doi.org/10.18632/aging.101937
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author Sun, Chao
Zhang, Shanshan
Wang, Jue
Jiang, Wen
Xin, Qian
Chen, Xiaojing
Zhang, Zhaohua
Luan, Yun
author_facet Sun, Chao
Zhang, Shanshan
Wang, Jue
Jiang, Wen
Xin, Qian
Chen, Xiaojing
Zhang, Zhaohua
Luan, Yun
author_sort Sun, Chao
collection PubMed
description Bronchopulmonary dysplasia (BPD) is the most common type of chronic lung disease in infancy; however, there is no effective treatment for it. In the present study, a neonatal mouse BPD model was established by continuous exposure to high oxygen (HO) levels. Mice were divided randomly into 5 groups: control, BPD, EPO, MSCs, and MSCs+EPO. At 2 weeks post-treatment, vessel density and the expression levels of endothelial growth factor (VEGF), stromal cell-derived factor-1 (SDF-1), and its receptor C-X-C chemokine receptor type 4 (CXCR4) were significantly increased in the MSC+EPO group compared with the EPO or MSCs group alone; moreover, EPO significantly enhanced MSCs proliferation, migration, and anti-apoptosis ability in vitro. Furthermore, the MSCs could differentiate into cells that were positive for the type II alveolar epithelial cell (AECII)-specific marker surfactant protein-C, but not positive for the AECI-specific marker aquaporin 5. Our present results suggested that MSCs in combination with EPO could significantly attenuate lung injury in a neonatal mouse model of BPD. The mechanism may be by the indirect promotion of angiogenesis, which may involve the SDF-1/CXCR4 axis.
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spelling pubmed-65199972019-05-29 EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis Sun, Chao Zhang, Shanshan Wang, Jue Jiang, Wen Xin, Qian Chen, Xiaojing Zhang, Zhaohua Luan, Yun Aging (Albany NY) Research Paper Bronchopulmonary dysplasia (BPD) is the most common type of chronic lung disease in infancy; however, there is no effective treatment for it. In the present study, a neonatal mouse BPD model was established by continuous exposure to high oxygen (HO) levels. Mice were divided randomly into 5 groups: control, BPD, EPO, MSCs, and MSCs+EPO. At 2 weeks post-treatment, vessel density and the expression levels of endothelial growth factor (VEGF), stromal cell-derived factor-1 (SDF-1), and its receptor C-X-C chemokine receptor type 4 (CXCR4) were significantly increased in the MSC+EPO group compared with the EPO or MSCs group alone; moreover, EPO significantly enhanced MSCs proliferation, migration, and anti-apoptosis ability in vitro. Furthermore, the MSCs could differentiate into cells that were positive for the type II alveolar epithelial cell (AECII)-specific marker surfactant protein-C, but not positive for the AECI-specific marker aquaporin 5. Our present results suggested that MSCs in combination with EPO could significantly attenuate lung injury in a neonatal mouse model of BPD. The mechanism may be by the indirect promotion of angiogenesis, which may involve the SDF-1/CXCR4 axis. Impact Journals 2019-04-29 /pmc/articles/PMC6519997/ /pubmed/31035257 http://dx.doi.org/10.18632/aging.101937 Text en Copyright © 2019 Sun et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution (CC BY) 3.0 License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Paper
Sun, Chao
Zhang, Shanshan
Wang, Jue
Jiang, Wen
Xin, Qian
Chen, Xiaojing
Zhang, Zhaohua
Luan, Yun
EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis
title EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis
title_full EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis
title_fullStr EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis
title_full_unstemmed EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis
title_short EPO enhances the protective effects of MSCs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis
title_sort epo enhances the protective effects of mscs in experimental hyperoxia-induced neonatal mice by promoting angiogenesis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6519997/
https://www.ncbi.nlm.nih.gov/pubmed/31035257
http://dx.doi.org/10.18632/aging.101937
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