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Fig. 3 | Arthritis Research & Therapy

Fig. 3

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. 3

Regulation of BMP pathway components by pro-inflammatory cytokines. Rheumatoid arthritis synoviocytes were cultured in media alone (CTRL) or in the presence of IL-17 (50 ng/mL) or TNF-α (0.5 ng/mL) or both. a-d Expression of several BMP pathway components, including a BMP receptors, b BMP ligands, c Smad protein family components and d BMP antagonists, was studied by quantitative reverse transcription-polymerase chain reaction after 12 h of culture. GNB2L1 was used as an endogenous control. Results represent increments in respect to cultures in media alone. The mean (± standard deviation) of three independent experiments is shown. ACTRIA type IA activin receptor, ACTRIIA type IIA activin receptor, ACTRIIB type IIB activin receptor, BAMBI bone morphogenetic protein and activin membrane-bound inhibitor, BMP bone morphogenetic protein, BMPRIA type IA bone morphogenetic protein receptor, BMPRIB type IB bone morphogenetic protein receptor, BMPRII type II bone morphogenetic protein receptor, CTRL control, IL-17 interleukin-17, Smad small mother against decapentaplegic homolog, TNF-α tumor necrosis factor-alpha

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