期刊
INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES
卷 19, 期 1, 页码 -出版社
MDPI
DOI: 10.3390/ijms19010190
关键词
visfatin; IL-6; TNF-; osteoarthritis; miR-199a-5p
资金
- Ministry of Science and Technology of Taiwan [MOST106-2320-B-029-002-, MOST106-2632-B-029-001-]
- China Medical University [CMU106-ASIA-03]
Osteoarthritis (OA), an inflammatory form of arthritis, is characterized by synovial inflammation and cartilage destruction largely influenced by two key proinflammatory cytokinesinterleukin-6 (IL-6) and tumor necrosis factor (TNF-). Notably, levels of visfatin (a proinflammatory adipokine) are elevated in patients with OA, although the relationship of visfatin to IL-6 and TNF- expression in OA pathogenesis has been unclear. In this study, visfatin enhanced the expression of IL-6 and TNF- 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- production. Moreover, transfection with miR-199a-5p mimics reversed visfatin-induced increases in IL-6 and TNF- production. Furthermore, we also found that visfatin-promoted IL-6 and TNF- 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.
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