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|Title: ||Visfatin Promotes IL-6 and TNF-α Production in Human Synovial Fibroblasts by Repressing miR-199a-5p through ERK, p38 and JNK Signaling Pathways|
|Authors: ||Wu, Min-Huan;Wu, Min-Huan;Tsa, Chun-Hao;Tsai, Chun-Hao;黃元勵;HUANG, YUAN-LI;Fong, Yi-Chin;Fong, Yi-Chin;湯智昕;Chih-Hsin, Tang;*|
|Issue Date: ||2018-08-20 09:44:37 (UTC+8)|
|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.
Keywords: visfatin, IL-6, TNF-α, osteoarthritis, miR-199a-5p
|Relation: ||International Journal of Medical Sciences|
|Appears in Collections:||[生物科技學系] 期刊論文|
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