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Fig. 4 | Arthritis Research & Therapy

Fig. 4

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. 4

Effects of BMP signaling blockade on TNF-α- and IL-17-induced cytokine and chemokine mRNA and protein expression in RA synoviocytes. RA synoviocytes were simultaneously treated with the BMP pathway inhibitor DMH1 and IL-17 (50 ng/mL) or TNF-α (0.5 ng/mL) or both. a After 12 h, mRNA levels were analyzed by quantitative reverse transcription-polymerase chain reaction. Cells were left untreated as control, and the fold induction is shown for each treatment. GNB2L1 was used as an endogenous control. Bars represent the mean (± SD) of four to six independent experiments. Asterisks represent statistically significant differences between DMH1-treated and DMH1-non-treated cells (*P ≤0.05; **P ≤0.01; ***P ≤0.005; by Mann–Whitney test). b Protein levels were determined by enzyme-linked immunosorbent assay/Cytometric Bead Array assays. Data shown are expressed as fold induction compared with the untreated condition. Asterisks represent statistically significant differences between DMH1-treated and DMH1-non-treated cells (*P ≤0.05; **P ≤0.01; ***P ≤0.005; by t test). Bars represent the mean (± SD) of three to five independent experiments. BMP bone morphogenetic protein, CTRL control, DMH1 dorsomorphin homologue 1, GM-CSF granulocyte-macrophage colony-stimulating factor, IL interleukin, MMP matrix metalloproteinase, RA rheumatoid arthritis, SD standard deviation, TNF-α tumor necrosis factor-alpha

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