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HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis
BACKGROUND: Osteoarthritis (OA) is a disabling joint disease that causes articular cartilage degeneration. It has been implicated that altered expression of histone deacetylase 2 (HDAC2) is found in patients with OA. However, the specific role of HDAC2 in the development of OA still remains enigmati...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7941997/ https://www.ncbi.nlm.nih.gov/pubmed/33750441 http://dx.doi.org/10.1186/s13075-020-02373-y |
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author | Wang, Zheng Zhou, Nan Wang, Wengang Yu, Yangke Xia, Lei Li, Ning |
author_facet | Wang, Zheng Zhou, Nan Wang, Wengang Yu, Yangke Xia, Lei Li, Ning |
author_sort | Wang, Zheng |
collection | PubMed |
description | BACKGROUND: Osteoarthritis (OA) is a disabling joint disease that causes articular cartilage degeneration. It has been implicated that altered expression of histone deacetylase 2 (HDAC2) is found in patients with OA. However, the specific role of HDAC2 in the development of OA still remains enigmatic. Hence, we sought to characterize the functional relevance of HDAC2 in the development of OA. METHODS: Anterior cruciate ligament surgery was performed to generate the rat model of OA. Luciferase assay was performed to evaluate the relationship between microRNA-503-5p (miR-503-5p) and serum- and glucocorticoid-inducible kinase-1 (SGK1). Functional experiments were conducted to examine the functional significance of miR-503-5p, histone deacetylase 2 (HDAC2), and SGK1 on the progression of OA by determining proliferation, apoptosis, and expression of apoptosis-associated proteins and inflammatory cytokines. RESULTS: HDAC2 could inhibit miR-503-5p expression. SGK1 was the target gene of miR-503-5p. Upregulation of miR-503-5p or silencing of HDAC2 contributed to enhanced proliferation, suppressed apoptosis (reduced expression of Caspase-3 and Bax but elevated expression of Bcl2), and promoted inflammation in chondrocytes of OA rats. CONCLUSION: In conclusion, our study demonstrated that HDAC2 could promote OA through miR-503-5p/SGK1 axis, which might function as a therapeutic target for OA treatment. |
format | Online Article Text |
id | pubmed-7941997 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-79419972021-03-10 HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis Wang, Zheng Zhou, Nan Wang, Wengang Yu, Yangke Xia, Lei Li, Ning Arthritis Res Ther Research Article BACKGROUND: Osteoarthritis (OA) is a disabling joint disease that causes articular cartilage degeneration. It has been implicated that altered expression of histone deacetylase 2 (HDAC2) is found in patients with OA. However, the specific role of HDAC2 in the development of OA still remains enigmatic. Hence, we sought to characterize the functional relevance of HDAC2 in the development of OA. METHODS: Anterior cruciate ligament surgery was performed to generate the rat model of OA. Luciferase assay was performed to evaluate the relationship between microRNA-503-5p (miR-503-5p) and serum- and glucocorticoid-inducible kinase-1 (SGK1). Functional experiments were conducted to examine the functional significance of miR-503-5p, histone deacetylase 2 (HDAC2), and SGK1 on the progression of OA by determining proliferation, apoptosis, and expression of apoptosis-associated proteins and inflammatory cytokines. RESULTS: HDAC2 could inhibit miR-503-5p expression. SGK1 was the target gene of miR-503-5p. Upregulation of miR-503-5p or silencing of HDAC2 contributed to enhanced proliferation, suppressed apoptosis (reduced expression of Caspase-3 and Bax but elevated expression of Bcl2), and promoted inflammation in chondrocytes of OA rats. CONCLUSION: In conclusion, our study demonstrated that HDAC2 could promote OA through miR-503-5p/SGK1 axis, which might function as a therapeutic target for OA treatment. BioMed Central 2021-03-09 2021 /pmc/articles/PMC7941997/ /pubmed/33750441 http://dx.doi.org/10.1186/s13075-020-02373-y 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 Article Wang, Zheng Zhou, Nan Wang, Wengang Yu, Yangke Xia, Lei Li, Ning HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis |
title | HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis |
title_full | HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis |
title_fullStr | HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis |
title_full_unstemmed | HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis |
title_short | HDAC2 interacts with microRNA-503-5p to regulate SGK1 in osteoarthritis |
title_sort | hdac2 interacts with microrna-503-5p to regulate sgk1 in osteoarthritis |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7941997/ https://www.ncbi.nlm.nih.gov/pubmed/33750441 http://dx.doi.org/10.1186/s13075-020-02373-y |
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