IL-17 Facilitates VCAM-1 Production and Monocyte Adhesion in Osteoarthritis Synovial Fibroblasts by Suppressing miR-5701 Synthesis
Osteoarthritis (OA) is characterized by the infiltration and adhesion of monocytes into the inflamed joint synovium. Interleukin (IL)-17 is a critical inflammatory mediator that participates in the progression of OA, although the mechanisms linking IL-17 and monocyte infiltration are not well unders...
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MDPI AG
2022-06-01
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author | Tsung-Ju Wu Sunny Li-Yun Chang Chih-Yang Lin Chao-Yang Lai Xiu-Yuan He Chun-Hao Tsai Chih-Yuan Ko Yi-Chin Fong Chen-Ming Su Chih-Hsin Tang |
author_facet | Tsung-Ju Wu Sunny Li-Yun Chang Chih-Yang Lin Chao-Yang Lai Xiu-Yuan He Chun-Hao Tsai Chih-Yuan Ko Yi-Chin Fong Chen-Ming Su Chih-Hsin Tang |
author_sort | Tsung-Ju Wu |
collection | DOAJ |
description | Osteoarthritis (OA) is characterized by the infiltration and adhesion of monocytes into the inflamed joint synovium. Interleukin (IL)-17 is a critical inflammatory mediator that participates in the progression of OA, although the mechanisms linking IL-17 and monocyte infiltration are not well understood. Our analysis of synovial tissue samples retrieved from the Gene Expression Omnibus (GEO) dataset exhibited higher monocyte marker (CD11b) and vascular cell adhesion molecule 1 (VCAM-1) levels in OA samples than in normal, healthy samples. The stimulation of human OA synovial fibroblasts (OASFs) with IL-17 increased VCAM-1 production and subsequently enhanced monocyte adhesion. IL-17 affected VCAM-1-dependent monocyte adhesion by reducing miR-5701 expression through the protein kinase C (PKC)-α and c-Jun N-terminal kinase (JNK) signaling cascades. Our findings improve our understanding about the effect of IL-17 on OA progression and, in particular, VCAM-1 production and monocyte adhesion, which may help with the design of more effective OA treatments. |
first_indexed | 2024-03-09T23:32:27Z |
format | Article |
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institution | Directory Open Access Journal |
issn | 1661-6596 1422-0067 |
language | English |
last_indexed | 2024-03-09T23:32:27Z |
publishDate | 2022-06-01 |
publisher | MDPI AG |
record_format | Article |
series | International Journal of Molecular Sciences |
spelling | doaj.art-babded2c57574681a221f4faf4d6f92d2023-11-23T17:07:06ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672022-06-012312680410.3390/ijms23126804IL-17 Facilitates VCAM-1 Production and Monocyte Adhesion in Osteoarthritis Synovial Fibroblasts by Suppressing miR-5701 SynthesisTsung-Ju Wu0Sunny Li-Yun Chang1Chih-Yang Lin2Chao-Yang Lai3Xiu-Yuan He4Chun-Hao Tsai5Chih-Yuan Ko6Yi-Chin Fong7Chen-Ming Su8Chih-Hsin Tang9Department of Physical Medicine and Rehabilitation, Changhua Christian Hospital, Changhua 500209, TaiwanGraduate Institute of Biomedical Sciences, China Medical University, Taichung 404333, TaiwanTranslational Medicine Center, Shin-Kong Wu Ho-Su Memorial Hospital, Taipei 111045, TaiwanDepartment of Medical Laboratory Science and Biotechnology, Asia University, Taichung 413305, TaiwanGraduate Institute of Biomedical Sciences, China Medical University, Taichung 404333, TaiwanDepartment of Sports Medicine, College of Health Care, China Medical University, Taichung 406040, TaiwanDepartment of Orthopedic Surgery, China Medical University Hospital, Taichung 404327, TaiwanDepartment of Sports Medicine, College of Health Care, China Medical University, Taichung 406040, TaiwanDepartment of Sports Medicine, College of Health Care, China Medical University, Taichung 406040, TaiwanGraduate Institute of Biomedical Sciences, China Medical University, Taichung 404333, TaiwanOsteoarthritis (OA) is characterized by the infiltration and adhesion of monocytes into the inflamed joint synovium. Interleukin (IL)-17 is a critical inflammatory mediator that participates in the progression of OA, although the mechanisms linking IL-17 and monocyte infiltration are not well understood. Our analysis of synovial tissue samples retrieved from the Gene Expression Omnibus (GEO) dataset exhibited higher monocyte marker (CD11b) and vascular cell adhesion molecule 1 (VCAM-1) levels in OA samples than in normal, healthy samples. The stimulation of human OA synovial fibroblasts (OASFs) with IL-17 increased VCAM-1 production and subsequently enhanced monocyte adhesion. IL-17 affected VCAM-1-dependent monocyte adhesion by reducing miR-5701 expression through the protein kinase C (PKC)-α and c-Jun N-terminal kinase (JNK) signaling cascades. Our findings improve our understanding about the effect of IL-17 on OA progression and, in particular, VCAM-1 production and monocyte adhesion, which may help with the design of more effective OA treatments.https://www.mdpi.com/1422-0067/23/12/6804IL-17osteoarthritismonocytesVCAM-1adhesion |
spellingShingle | Tsung-Ju Wu Sunny Li-Yun Chang Chih-Yang Lin Chao-Yang Lai Xiu-Yuan He Chun-Hao Tsai Chih-Yuan Ko Yi-Chin Fong Chen-Ming Su Chih-Hsin Tang IL-17 Facilitates VCAM-1 Production and Monocyte Adhesion in Osteoarthritis Synovial Fibroblasts by Suppressing miR-5701 Synthesis International Journal of Molecular Sciences IL-17 osteoarthritis monocytes VCAM-1 adhesion |
title | IL-17 Facilitates VCAM-1 Production and Monocyte Adhesion in Osteoarthritis Synovial Fibroblasts by Suppressing miR-5701 Synthesis |
title_full | IL-17 Facilitates VCAM-1 Production and Monocyte Adhesion in Osteoarthritis Synovial Fibroblasts by Suppressing miR-5701 Synthesis |
title_fullStr | IL-17 Facilitates VCAM-1 Production and Monocyte Adhesion in Osteoarthritis Synovial Fibroblasts by Suppressing miR-5701 Synthesis |
title_full_unstemmed | IL-17 Facilitates VCAM-1 Production and Monocyte Adhesion in Osteoarthritis Synovial Fibroblasts by Suppressing miR-5701 Synthesis |
title_short | IL-17 Facilitates VCAM-1 Production and Monocyte Adhesion in Osteoarthritis Synovial Fibroblasts by Suppressing miR-5701 Synthesis |
title_sort | il 17 facilitates vcam 1 production and monocyte adhesion in osteoarthritis synovial fibroblasts by suppressing mir 5701 synthesis |
topic | IL-17 osteoarthritis monocytes VCAM-1 adhesion |
url | https://www.mdpi.com/1422-0067/23/12/6804 |
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