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MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1

In this study, miR-19b-3p was downregulated in osteoarthritic cartilage tissues and IL-1β-stimulated primary chondrocytes, and miR-19b-3p overexpression reversed the inhibitory effect of IL-1β on cell viability, the promotion effects of apoptosis, inflammatory factor secretion and extracellular matr...

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Detalles Bibliográficos
Autores principales: Shi, Liang, Duan, Liang, Duan, Dapeng, Fan, Yayi, Xu, Honghai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9578845/
https://www.ncbi.nlm.nih.gov/pubmed/36267095
http://dx.doi.org/10.1155/2022/5133754
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author Shi, Liang
Duan, Liang
Duan, Dapeng
Fan, Yayi
Xu, Honghai
author_facet Shi, Liang
Duan, Liang
Duan, Dapeng
Fan, Yayi
Xu, Honghai
author_sort Shi, Liang
collection PubMed
description In this study, miR-19b-3p was downregulated in osteoarthritic cartilage tissues and IL-1β-stimulated primary chondrocytes, and miR-19b-3p overexpression reversed the inhibitory effect of IL-1β on cell viability, the promotion effects of apoptosis, inflammatory factor secretion and extracellular matrix degradation, whereas the opposite effect was observed with miR-19b-3p inhibitor. Moreover, SOCS1 is a target gene of miR-19b-3p. Furthermore, SOCS1 overexpression enhanced cell injury compared with IL-1β alone treatment, whereas knockdown of SOCS1 restored cell damage caused by IL-1β. Further studies revealed that miR-19b-3p promoted chondrocyte injury repair by suppressing SOCS1 expression, and we found that was mediated by blocking the MAPK/NF-κB axis. Taken together, our findings may provide a new therapeutic strategy for osteoarthritis.
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spelling pubmed-95788452022-10-19 MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1 Shi, Liang Duan, Liang Duan, Dapeng Fan, Yayi Xu, Honghai Evid Based Complement Alternat Med Research Article In this study, miR-19b-3p was downregulated in osteoarthritic cartilage tissues and IL-1β-stimulated primary chondrocytes, and miR-19b-3p overexpression reversed the inhibitory effect of IL-1β on cell viability, the promotion effects of apoptosis, inflammatory factor secretion and extracellular matrix degradation, whereas the opposite effect was observed with miR-19b-3p inhibitor. Moreover, SOCS1 is a target gene of miR-19b-3p. Furthermore, SOCS1 overexpression enhanced cell injury compared with IL-1β alone treatment, whereas knockdown of SOCS1 restored cell damage caused by IL-1β. Further studies revealed that miR-19b-3p promoted chondrocyte injury repair by suppressing SOCS1 expression, and we found that was mediated by blocking the MAPK/NF-κB axis. Taken together, our findings may provide a new therapeutic strategy for osteoarthritis. Hindawi 2022-10-11 /pmc/articles/PMC9578845/ /pubmed/36267095 http://dx.doi.org/10.1155/2022/5133754 Text en Copyright © 2022 Liang Shi et al. https://creativecommons.org/licenses/by/4.0/This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Shi, Liang
Duan, Liang
Duan, Dapeng
Fan, Yayi
Xu, Honghai
MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1
title MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1
title_full MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1
title_fullStr MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1
title_full_unstemmed MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1
title_short MiR-19b-3p Attenuates Chondrocytes Injury by Inhibiting MAPK/NF-Κb Axis via Targeting SOCS1
title_sort mir-19b-3p attenuates chondrocytes injury by inhibiting mapk/nf-κb axis via targeting socs1
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9578845/
https://www.ncbi.nlm.nih.gov/pubmed/36267095
http://dx.doi.org/10.1155/2022/5133754
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