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Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT

BACKGROUND: Osteoarthritis (OA) remains one of the most common osteopathy for centuries, which can be attributed to multiple risk factors including mechanical and biochemical ones. More and more studies verified that inflammatory cytokines play important roles in the progression of OA, such as tumor...

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Autores principales: Zhang, Qiang, Ouyang, Zhengxiao, song, Xiaoxia, Zhu, Wei, Tang, Xinqiao, Liu, Zhong, Chen, Xiaoming
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Lippincott Williams & Wilkins 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8702089/
https://www.ncbi.nlm.nih.gov/pubmed/34941032
http://dx.doi.org/10.1097/MD.0000000000027868
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author Zhang, Qiang
Ouyang, Zhengxiao
song, Xiaoxia
Zhu, Wei
Tang, Xinqiao
Liu, Zhong
Chen, Xiaoming
author_facet Zhang, Qiang
Ouyang, Zhengxiao
song, Xiaoxia
Zhu, Wei
Tang, Xinqiao
Liu, Zhong
Chen, Xiaoming
author_sort Zhang, Qiang
collection PubMed
description BACKGROUND: Osteoarthritis (OA) remains one of the most common osteopathy for centuries, which can be attributed to multiple risk factors including mechanical and biochemical ones. More and more studies verified that inflammatory cytokines play important roles in the progression of OA, such as tumor necrosis factor-alpha (TNF-α). In this study, we aimed to investigate the relationship between epigenetic manifestations of TNF-? and the pathogenesis of OA. METHODS: Totally, 37 OA patients’ cartilage was collected through the knee joint and 13 samples of articular cartilage as healthy control was collected through traumatic amputation. Real-time PCR, Western blot and ELISA analysis were performed to observe the expression of target genes and proteins in collected samples. RESULTS: Compared with the healthy control group, TNF-? was over-expressing in cartilage which was collected from OA patients. DNA hypomethylation, histone hyperacetylation and histone methylation were observed in the TNF-? promoter in OA compared with normal patients, and we also studied series of enzymes associated with epigenetics. The results showed that by increasing DNA methylation and decreasing histone acetylation in the TNF-? promoter, and TNF-? over-expression in OA cartilage was suppressed, histone methylation has no significant correlation with OA. CONCLUSION: In conclusion, the changes of epigenetic status regulate TNF-α expression in the cells, which are pivotal to the OA disease process. These results may give us a better understanding of OA and may provide new therapeutic options.
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spelling pubmed-87020892021-12-27 Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT Zhang, Qiang Ouyang, Zhengxiao song, Xiaoxia Zhu, Wei Tang, Xinqiao Liu, Zhong Chen, Xiaoming Medicine (Baltimore) 3700 BACKGROUND: Osteoarthritis (OA) remains one of the most common osteopathy for centuries, which can be attributed to multiple risk factors including mechanical and biochemical ones. More and more studies verified that inflammatory cytokines play important roles in the progression of OA, such as tumor necrosis factor-alpha (TNF-α). In this study, we aimed to investigate the relationship between epigenetic manifestations of TNF-? and the pathogenesis of OA. METHODS: Totally, 37 OA patients’ cartilage was collected through the knee joint and 13 samples of articular cartilage as healthy control was collected through traumatic amputation. Real-time PCR, Western blot and ELISA analysis were performed to observe the expression of target genes and proteins in collected samples. RESULTS: Compared with the healthy control group, TNF-? was over-expressing in cartilage which was collected from OA patients. DNA hypomethylation, histone hyperacetylation and histone methylation were observed in the TNF-? promoter in OA compared with normal patients, and we also studied series of enzymes associated with epigenetics. The results showed that by increasing DNA methylation and decreasing histone acetylation in the TNF-? promoter, and TNF-? over-expression in OA cartilage was suppressed, histone methylation has no significant correlation with OA. CONCLUSION: In conclusion, the changes of epigenetic status regulate TNF-α expression in the cells, which are pivotal to the OA disease process. These results may give us a better understanding of OA and may provide new therapeutic options. Lippincott Williams & Wilkins 2021-12-23 /pmc/articles/PMC8702089/ /pubmed/34941032 http://dx.doi.org/10.1097/MD.0000000000027868 Text en Copyright © 2021 the Author(s). Published by Wolters Kluwer Health, Inc. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License 4.0 (CCBY), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. http://creativecommons.org/licenses/by/4.0 (https://creativecommons.org/licenses/by/4.0/)
spellingShingle 3700
Zhang, Qiang
Ouyang, Zhengxiao
song, Xiaoxia
Zhu, Wei
Tang, Xinqiao
Liu, Zhong
Chen, Xiaoming
Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT
title Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT
title_full Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT
title_fullStr Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT
title_full_unstemmed Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT
title_short Epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - CONSORT
title_sort epigenetic modifications of tumor necrosis factor-alpha in joint cartilage tissue from osteoarthritis patients - consort
topic 3700
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8702089/
https://www.ncbi.nlm.nih.gov/pubmed/34941032
http://dx.doi.org/10.1097/MD.0000000000027868
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