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MiR-206 regulates the progression of osteoporosis via targeting HDAC4

BACKGROUND: More and more studies have confirmed that miRNAs play an important role in maintaining bone remodeling and bone metabolism. This study investigated the expression level of miR-206 in the serum of osteoporosis (OP) patients and explored the effect and mechanism of miR-206 on the occurrenc...

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Autores principales: Lu, Zhiyuan, Wang, Dawei, Wang, Xuming, Zou, Jilong, Sun, Jiabing, Bi, Zhenggang
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812640/
https://www.ncbi.nlm.nih.gov/pubmed/33461610
http://dx.doi.org/10.1186/s40001-021-00480-3
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author Lu, Zhiyuan
Wang, Dawei
Wang, Xuming
Zou, Jilong
Sun, Jiabing
Bi, Zhenggang
author_facet Lu, Zhiyuan
Wang, Dawei
Wang, Xuming
Zou, Jilong
Sun, Jiabing
Bi, Zhenggang
author_sort Lu, Zhiyuan
collection PubMed
description BACKGROUND: More and more studies have confirmed that miRNAs play an important role in maintaining bone remodeling and bone metabolism. This study investigated the expression level of miR-206 in the serum of osteoporosis (OP) patients and explored the effect and mechanism of miR-206 on the occurrence and development of osteoporosis. METHODS: 120 postmenopausal women were recruited, including 63 cases with OP and 57 women without OP. The levels of miR-206 were determined by qRT-PCR technology. Spearman correlation coefficient was used to evaluate the correlation of miR-206 with bone mineral density (BMD). An ROC curve was used to evaluate the diagnostic value of miR-206 in osteoporosis. The effects of miR-206 on cell proliferation and cell apoptosis of hFOBs were measured by CCK-8 assay and flow cytometry, respectively. Luciferase reporter gene assay was used to confirm the interaction of miR-206 and the 3′UTR of HDAC4. RESULTS: Serum miR-206 had low expression level in osteoporosis patient group compared with control group. The expression level of serum miR-206 had diagnostic value for osteoporosis, and the serum miR-206 levels were positively correlated with BMD. The down-regulated miR-206 could inhibit cell proliferation and promote cell apoptosis. Luciferase analysis indicated that HDAC4 was the target gene of miR-206. CONCLUSIONS: MiR-206 could be used as a new potential diagnostic biomarker for osteoporosis, and in in vitro cell experiments, miR-206 may regulate osteoblast cell proliferation and apoptosis by targeting HDAC4.
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spelling pubmed-78126402021-01-19 MiR-206 regulates the progression of osteoporosis via targeting HDAC4 Lu, Zhiyuan Wang, Dawei Wang, Xuming Zou, Jilong Sun, Jiabing Bi, Zhenggang Eur J Med Res Research BACKGROUND: More and more studies have confirmed that miRNAs play an important role in maintaining bone remodeling and bone metabolism. This study investigated the expression level of miR-206 in the serum of osteoporosis (OP) patients and explored the effect and mechanism of miR-206 on the occurrence and development of osteoporosis. METHODS: 120 postmenopausal women were recruited, including 63 cases with OP and 57 women without OP. The levels of miR-206 were determined by qRT-PCR technology. Spearman correlation coefficient was used to evaluate the correlation of miR-206 with bone mineral density (BMD). An ROC curve was used to evaluate the diagnostic value of miR-206 in osteoporosis. The effects of miR-206 on cell proliferation and cell apoptosis of hFOBs were measured by CCK-8 assay and flow cytometry, respectively. Luciferase reporter gene assay was used to confirm the interaction of miR-206 and the 3′UTR of HDAC4. RESULTS: Serum miR-206 had low expression level in osteoporosis patient group compared with control group. The expression level of serum miR-206 had diagnostic value for osteoporosis, and the serum miR-206 levels were positively correlated with BMD. The down-regulated miR-206 could inhibit cell proliferation and promote cell apoptosis. Luciferase analysis indicated that HDAC4 was the target gene of miR-206. CONCLUSIONS: MiR-206 could be used as a new potential diagnostic biomarker for osteoporosis, and in in vitro cell experiments, miR-206 may regulate osteoblast cell proliferation and apoptosis by targeting HDAC4. BioMed Central 2021-01-18 /pmc/articles/PMC7812640/ /pubmed/33461610 http://dx.doi.org/10.1186/s40001-021-00480-3 Text en © The Author(s) 2021 Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. 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 in a credit line to the data.
spellingShingle Research
Lu, Zhiyuan
Wang, Dawei
Wang, Xuming
Zou, Jilong
Sun, Jiabing
Bi, Zhenggang
MiR-206 regulates the progression of osteoporosis via targeting HDAC4
title MiR-206 regulates the progression of osteoporosis via targeting HDAC4
title_full MiR-206 regulates the progression of osteoporosis via targeting HDAC4
title_fullStr MiR-206 regulates the progression of osteoporosis via targeting HDAC4
title_full_unstemmed MiR-206 regulates the progression of osteoporosis via targeting HDAC4
title_short MiR-206 regulates the progression of osteoporosis via targeting HDAC4
title_sort mir-206 regulates the progression of osteoporosis via targeting hdac4
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7812640/
https://www.ncbi.nlm.nih.gov/pubmed/33461610
http://dx.doi.org/10.1186/s40001-021-00480-3
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