Fig. 4: Melatonin upregulated miR-185a expression and attenuated proinflammatory factor production. | Cell Death & Disease

Fig. 4: Melatonin upregulated miR-185a expression and attenuated proinflammatory factor production.

From: Melatonin abolished proinflammatory factor expression and antagonized osteoarthritis progression in vivo

Fig. 4

A Using 4 open-source software databases, we predicted that 11 miRs could bind the 3’-UTRs of TNF-α, IL-8, and VEGF. After treating OASFs with melatonin (1 mM) for 24 h, miR levels were measured (n = 6). B OASFs were treated with different concentrations of melatonin for 24 h, then analyzed by qPCR for miR-185a expression (n = 6). C–F OASFs were transfected with the miR-185a inhibitor for 24 h then incubated with 1 mM of melatonin. qPCR (n = 6), western blot (n = 3) and ELISA (n = 9) assays determined TNF-α, IL-8, and VEGF levels, respectively. G, H OASFs were transfected with the indicated WT (G) or MT (H) luciferase plasmids, with or without the miR-185a inhibitor, then stimulated with melatonin (1 mM). Relative luciferase activity (n = 6) was determined. I OASFs were treated with activators (740-YP, SC-79, or ceramide C6) for 30 min then incubated with 1 mM of melatonin. The qPCR assay (n = 6) quantified miR-185a expression. Error bars indicate means ± S.D. *p < 0.05 versus controls; #p < 0.05 versus the melatonin-treated group.

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