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miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways

In this study, we sought to investigate the expression of microRNA (miR)-214 on the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) and explore the possible underlying mechanisms. We found that the overexpression of miR-214 effectively promoted the adipocyte differen...

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Autores principales: Guo, Yongzhi, Li, Lianhua, Gao, Jie, Chen, Xiaobin, Sang, Qinghua
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5179177/
https://www.ncbi.nlm.nih.gov/pubmed/27959394
http://dx.doi.org/10.3892/ijmm.2016.2826
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author Guo, Yongzhi
Li, Lianhua
Gao, Jie
Chen, Xiaobin
Sang, Qinghua
author_facet Guo, Yongzhi
Li, Lianhua
Gao, Jie
Chen, Xiaobin
Sang, Qinghua
author_sort Guo, Yongzhi
collection PubMed
description In this study, we sought to investigate the expression of microRNA (miR)-214 on the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) and explore the possible underlying mechanisms. We found that the overexpression of miR-214 effectively promoted the adipocyte differentiation of BMSCs in vitro, reduced alkaline phosphatase (ALP) activity and the gene expression of collagen type I (Col I), osteocalcin (OCN) and osteopontin (OPN) in the BMSCs. We further found that the overexpression of miR-214 suppressed the protein expression of fibroblast growth factor (FGF), phosphorylated c-Jun N-terminal kinase (p-JNK) and phosphorylated p38 (p-p38) in the BMSCs. The downregulation of miR-214 promoted the osteogenic differentiation of BMSCs, and increased ALP activity and Col I, OCN and OPN gene expression in the BMSCs. It also increased FGF p-JNK and p-p38 protein expression in the BMSCs. The use of JNK inhibitor (SP600125) enhanced the inhibitory effects of miR-214 overexpression on osteogenic differentiation, ALP activity, and Col I, OCN and OPN gene expression in the BMSCs. Lastly, the use of p38 inhibitor (SB202190) also enhanced the inhibitory effects of miR-214 overexpression on ALP activity, and Col I, OCN and OPN gene expression in the BMSCs. These results provide a mechanism responsible for the suppressive effects of miR-214 on the osteogenic differentiation of BMSCs involving the inhibition of the JNK and p38 pathways.
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spelling pubmed-51791772016-12-28 miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways Guo, Yongzhi Li, Lianhua Gao, Jie Chen, Xiaobin Sang, Qinghua Int J Mol Med Articles In this study, we sought to investigate the expression of microRNA (miR)-214 on the osteogenic differentiation of bone marrow-derived mesenchymal stem cells (BMSCs) and explore the possible underlying mechanisms. We found that the overexpression of miR-214 effectively promoted the adipocyte differentiation of BMSCs in vitro, reduced alkaline phosphatase (ALP) activity and the gene expression of collagen type I (Col I), osteocalcin (OCN) and osteopontin (OPN) in the BMSCs. We further found that the overexpression of miR-214 suppressed the protein expression of fibroblast growth factor (FGF), phosphorylated c-Jun N-terminal kinase (p-JNK) and phosphorylated p38 (p-p38) in the BMSCs. The downregulation of miR-214 promoted the osteogenic differentiation of BMSCs, and increased ALP activity and Col I, OCN and OPN gene expression in the BMSCs. It also increased FGF p-JNK and p-p38 protein expression in the BMSCs. The use of JNK inhibitor (SP600125) enhanced the inhibitory effects of miR-214 overexpression on osteogenic differentiation, ALP activity, and Col I, OCN and OPN gene expression in the BMSCs. Lastly, the use of p38 inhibitor (SB202190) also enhanced the inhibitory effects of miR-214 overexpression on ALP activity, and Col I, OCN and OPN gene expression in the BMSCs. These results provide a mechanism responsible for the suppressive effects of miR-214 on the osteogenic differentiation of BMSCs involving the inhibition of the JNK and p38 pathways. D.A. Spandidos 2017-01 2016-12-12 /pmc/articles/PMC5179177/ /pubmed/27959394 http://dx.doi.org/10.3892/ijmm.2016.2826 Text en Copyright: © Guo 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
Guo, Yongzhi
Li, Lianhua
Gao, Jie
Chen, Xiaobin
Sang, Qinghua
miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways
title miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways
title_full miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways
title_fullStr miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways
title_full_unstemmed miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways
title_short miR-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the JNK and p38 pathways
title_sort mir-214 suppresses the osteogenic differentiation of bone marrow-derived mesenchymal stem cells and these effects are mediated through the inhibition of the jnk and p38 pathways
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5179177/
https://www.ncbi.nlm.nih.gov/pubmed/27959394
http://dx.doi.org/10.3892/ijmm.2016.2826
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