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Fig. 6 | Arthritis Research & Therapy

Fig. 6

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. 6

Effects of exogenous BMP6 stimulation on cytokine, chemokine, and matrix metalloproteinase expression in RA synoviocytes. a The expression of the indicated pro-inflammatory factors was analyzed by qRT-PCR in RA synoviocytes cultured in media alone (CTRL) or supplemented with BMP6 (10 ng/mL) for 12 h. b RA synoviocyte cultures were treated with IL-17 (50 ng/mL) or TNF-α (0.5 ng/mL) or both in the presence or absence of BMP6. After 12 h, mRNA levels for the indicated factors were analyzed by qRT-PCR. 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 (± standard deviation) of four to six independent experiments. Asterisks represent statistically significant differences between BMP6-treated and -non-treated cells (*P ≤0.05; **P ≤0.01; ***P ≤0.005; by Mann–Whitney test). BMP bone morphogenetic protein, CCL2 chemokine (C-C motif) ligand 2, CCL5 chemokine (C-C motif) ligand 5, CTRL control, CXCL10 chemokine (C-X-C motif) ligand 10, GM-CSF granulocyte-macrophage colony-stimulating factor, IL interleukin, MMP matrix metalloproteinase, qRT-PCR quantitative reverse transcription-polymerase chain reaction, RA rheumatoid arthritis, TNF-α tumor necrosis factor-alpha

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