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Int. J. Mol. Sci. 2018, 19(1), 190; https://doi.org/10.3390/ijms19010190

Visfatin Promotes IL-6 and TNF-α Production in Human Synovial Fibroblasts by Repressing miR-199a-5p through ERK, p38 and JNK Signaling Pathways

1
Physical Education Office, Tunghai University, Taichung 40704, Taiwan
2
Sports Recreation and Health Management Continuing Studies, Tunghai University, Taichung 40704, Taiwan
3
School of Medicine, China Medical University, Taichung 40402, Taiwan
4
Department of Orthopedic Surgery, China Medical University Hospital, Taichung 40402, Taiwan
5
Department of Biotechnology, College of Health Science, Asia University, Taichung 41354, Taiwan
6
Department of Sports Medicine, College of Health Care, China Medical University, Taichung 40402, Taiwan
7
Department of Orthopaedic Surgery, China Medical University Beigang Hospital, Yun-Lin County 65152, Taiwan
8
Graduate Institute of Basic Medical Science, China Medical University, Taichung 40402, Taiwan
*
Author to whom correspondence should be addressed.
Received: 15 December 2017 / Revised: 29 December 2017 / Accepted: 4 January 2018 / Published: 8 January 2018
(This article belongs to the Special Issue Research of Pathogenesis and Novel Therapeutics in Arthritis)
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Abstract

Osteoarthritis (OA), an inflammatory form of arthritis, is characterized by synovial inflammation and cartilage destruction largely influenced by two key proinflammatory cytokines—interleukin-6 (IL-6) and tumor necrosis factor α (TNF-α). Notably, levels of visfatin (a proinflammatory adipokine) are elevated in patients with OA, although the relationship of visfatin to IL-6 and TNF-α expression in OA pathogenesis has been unclear. In this study, visfatin enhanced the expression of IL-6 and TNF-α in human OA synovial fibroblasts (OASFs) in a concentration-dependent manner and stimulation of OASFs with visfatin promoted phosphorylation of extracellular-signal-regulated kinase (ERK), p38, and c-Jun N-terminal kinase (JNK), while ERK, p38, and JNK inhibitors or siRNAs all abolished visfatin-induced increases in IL-6 and TNF-α production. Moreover, transfection with miR-199a-5p mimics reversed visfatin-induced increases in IL-6 and TNF-α production. Furthermore, we also found that visfatin-promoted IL-6 and TNF-α production is mediated via the inhibition of miR-199a-5p expression through the ERK, p38, and JNK signaling pathways. Visfatin may therefore be an appropriate target for drug intervention in OA treatment. View Full-Text
Keywords: visfatin; IL-6; TNF-α; osteoarthritis; miR-199a-5p visfatin; IL-6; TNF-α; osteoarthritis; miR-199a-5p
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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. (CC BY 4.0).
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Wu, M.-H.; Tsai, C.-H.; Huang, Y.-L.; Fong, Y.-C.; Tang, C.-H. Visfatin Promotes IL-6 and TNF-α Production in Human Synovial Fibroblasts by Repressing miR-199a-5p through ERK, p38 and JNK Signaling Pathways. Int. J. Mol. Sci. 2018, 19, 190.

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