Fig. 1

Treatment effect of Dexamethasone (DEX 40nM) on inflamed chondrocytes (mRNA, miRNA). (A) DEX 40nM treatment significantly reduced inflammation related genes like matrix metalloproteinase-1 (MMP-1: logFC=-1.91, FDR = 5.50E−01), matrix metalloproteinase-12 (MMP-12: logFC=−1.15, FDR = 8.80E−05), chitinase-3 like-protein-1 (CHI3L1: logFC=−0.50, FDR = 1.68E−03) and complement factor B (CFB: logFC=−1.15, FDR = 2.97E−04)). (B) Extracellular matrix (ECM)-related genes COL2A1 and ACAN showed similar significantly decreased expression in both DEX-treated and untreated inflamed chondrocytes compared to healthy controls at T48 (COL2A1: DEX treated: logFC=−5.28, FDR = 9.78E−08, untreated: logFC=−4.76, FDR = 3.56E−03; ACAN: DEX treated: logFC=−2.10 FDR = 1.53E−05, untreated: logFC=−2.28, FDR = 6.10E−03). (C) DEX treatment downregulated inflammation- related miRNAs miR-147-3p (T24: logFC=−0.13, FDR = 9.99E−01; T48: logFC=−0.29,FDR = 9.52E−01), miR-146a-5p (T24:logFC = 0.35,FDR = 9.99E−01; T48: logFC=−0.36, FDR = 9.52E−01), miR-146b-5p (T24: logFC=−0.35, FDR = 9.99E−01; T48: logFC=−0.36 ,FDR = 9.52E−01) and miR-34a-5p (T24: logFC = 0.08, FDR = 9.99E−01; T48: logFC=−0.08, FDR = 9.52E−015) compared to inflamed untreated controls. (D) DEX treatment significantly downregulated pro-regenerative miRNAs miR-140-3p (logFC=−0.73, FDR = 2.30E−02) and miR-1290 (logFC=−1, FDR = 2.40E−02) in DEX-treated cells compared to healthy chondrocytes at T48.