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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Blockade of bone morphogenetic protein signaling potentiates the pro-inflammatory phenotype induced by interleukin-17 and tumor necrosis factor-α combination in rheumatoid synoviocytes

Fig. 5

Effects of bone morphogenetic protein inhibitor DMH1 treatment on TNF-α and IL-17 combination-induced chemokine and matrix metalloproteinase mRNA expression in RA synoviocytes. Synoviocytes from patients with RA were left untreated (CTRL) or stimulated with IL-17 (50 ng/mL) or TNF-α (0.5 ng/mL) or both in the presence or absence of DMH1. The expression of a the indicated chemokines and b matrix metalloproteinases was analyzed by quantitative reverse transcription-polymerase chain reaction after 12 h of culture. GNB2L1 was used as an endogenous control. Fold induction relative to untreated cells is shown, and the mean (± standard deviation) of four to six independent experiments is presented. Asterisks represent statistically significant differences between DMH1-non-treated and DMH1-treated cells (*P ≤0.05; **P ≤0.01; ***P ≤0.005; by Mann–Whitney test). CCL2 chemokine (C-C motif) ligand 2, CCL5 chemokine (C-C motif) ligand 5, CTRL control, CXCL10 chemokine (C-X-C motif) ligand 10, DMH1 dorsomorphin homologue 1, IL-17 interleukin-17, MMP matrix metalloproteinase, RA rheumatoid arthritis, TNF-α tumor necrosis factor-alpha

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