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Hypoxia-induced MTA1 promotes MC3T3 osteoblast growth but suppresses MC3T3 osteoblast differentiation

BACKGROUND: Bone fracture is one of the most common physical injuries in which gene expression and the microenvironment are reprogramed to facilitate the recovery process. METHODS: By specific siRNA transfection and MTT assay, we evaluated the effects of metastasis-associated gene 1 (MTA1) in osteob...

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Autores principales: Liu, Tielong, Zou, Weiwei, Shi, Guodong, Xu, Jian, Zhang, Fei, Xiao, Jianru, Wang, Yan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4324858/
https://www.ncbi.nlm.nih.gov/pubmed/25644400
http://dx.doi.org/10.1186/s40001-015-0084-x
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author Liu, Tielong
Zou, Weiwei
Shi, Guodong
Xu, Jian
Zhang, Fei
Xiao, Jianru
Wang, Yan
author_facet Liu, Tielong
Zou, Weiwei
Shi, Guodong
Xu, Jian
Zhang, Fei
Xiao, Jianru
Wang, Yan
author_sort Liu, Tielong
collection PubMed
description BACKGROUND: Bone fracture is one of the most common physical injuries in which gene expression and the microenvironment are reprogramed to facilitate the recovery process. METHODS: By specific siRNA transfection and MTT assay, we evaluated the effects of metastasis-associated gene 1 (MTA1) in osteoblast growth. To show the role of MTA1 in osteoblast under hypoxia conditions, by overexpressing and silencing MTA1 expression, we performed mineral deposition and alkaline phosphatase activity assay to observe the differentiation status of osteoblast cells. Real-time PCR and Western blot assays were adopted to detect the expression of certain target genes. RESULTS: Here, we reported that hypoxia-induced MTA1 expression through hypoxia-induced factor 1 alpha (HIF-1α) and stimulated the growth of osteoblast MC3T3 cells. Silencing of MTA1 through specific siRNA suppressed MC3T3 cell growth and elicited cell differentiation and induced alkaline phosphatase activation and the upregulation of bone morphogenetic protein-2 and osteocalcin. CONCLUSIONS: We found that MTA1 was regulated by HIF-1α in hypoxia circumstance to suppress osteoblast differentiation. These findings provide new insights for bone fracture healing and new strategies to develop potential targets to promote fracture healing. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40001-015-0084-x) contains supplementary material, which is available to authorized users.
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spelling pubmed-43248582015-02-12 Hypoxia-induced MTA1 promotes MC3T3 osteoblast growth but suppresses MC3T3 osteoblast differentiation Liu, Tielong Zou, Weiwei Shi, Guodong Xu, Jian Zhang, Fei Xiao, Jianru Wang, Yan Eur J Med Res Research BACKGROUND: Bone fracture is one of the most common physical injuries in which gene expression and the microenvironment are reprogramed to facilitate the recovery process. METHODS: By specific siRNA transfection and MTT assay, we evaluated the effects of metastasis-associated gene 1 (MTA1) in osteoblast growth. To show the role of MTA1 in osteoblast under hypoxia conditions, by overexpressing and silencing MTA1 expression, we performed mineral deposition and alkaline phosphatase activity assay to observe the differentiation status of osteoblast cells. Real-time PCR and Western blot assays were adopted to detect the expression of certain target genes. RESULTS: Here, we reported that hypoxia-induced MTA1 expression through hypoxia-induced factor 1 alpha (HIF-1α) and stimulated the growth of osteoblast MC3T3 cells. Silencing of MTA1 through specific siRNA suppressed MC3T3 cell growth and elicited cell differentiation and induced alkaline phosphatase activation and the upregulation of bone morphogenetic protein-2 and osteocalcin. CONCLUSIONS: We found that MTA1 was regulated by HIF-1α in hypoxia circumstance to suppress osteoblast differentiation. These findings provide new insights for bone fracture healing and new strategies to develop potential targets to promote fracture healing. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s40001-015-0084-x) contains supplementary material, which is available to authorized users. BioMed Central 2015-02-03 /pmc/articles/PMC4324858/ /pubmed/25644400 http://dx.doi.org/10.1186/s40001-015-0084-x Text en © Liu et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Liu, Tielong
Zou, Weiwei
Shi, Guodong
Xu, Jian
Zhang, Fei
Xiao, Jianru
Wang, Yan
Hypoxia-induced MTA1 promotes MC3T3 osteoblast growth but suppresses MC3T3 osteoblast differentiation
title Hypoxia-induced MTA1 promotes MC3T3 osteoblast growth but suppresses MC3T3 osteoblast differentiation
title_full Hypoxia-induced MTA1 promotes MC3T3 osteoblast growth but suppresses MC3T3 osteoblast differentiation
title_fullStr Hypoxia-induced MTA1 promotes MC3T3 osteoblast growth but suppresses MC3T3 osteoblast differentiation
title_full_unstemmed Hypoxia-induced MTA1 promotes MC3T3 osteoblast growth but suppresses MC3T3 osteoblast differentiation
title_short Hypoxia-induced MTA1 promotes MC3T3 osteoblast growth but suppresses MC3T3 osteoblast differentiation
title_sort hypoxia-induced mta1 promotes mc3t3 osteoblast growth but suppresses mc3t3 osteoblast differentiation
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4324858/
https://www.ncbi.nlm.nih.gov/pubmed/25644400
http://dx.doi.org/10.1186/s40001-015-0084-x
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