Fig. 7

MiRNA-146a-5p inhibited proliferation of RA FLS, angiogenesis and delayed the disease progression on CIA mice, whereas CTGF promoted angiogenesis. a MTT assay. RA FLS were transfected with miR146a-5p-mimics and negative control (NC), and the proliferation ability was determined. b, d Endothelial tube formation assay. HUVEC were transfected with miR146a-5p-mimics negative control (NC), miR146a-5p-mimics, CTGF siRNA negative control (iNC), and CTGF siRNA oligo. Tube formation was photographed (left panel). The number of intersections among branches of assembled HUVEC networks was calculated in the whole field (right panel). c, e CAM assay. CAM were treated with miR146a-5p-agomir negative control (NC), chick miR146a-5p-agomir, control RNAi, and a lentiviral vector harboring RNAi sequence targeting the CTGF gene (CTGF RNAi). CAMs were examined and photographed (left panel). The percentage of angiogenic area (right panel) was calculated. n = 10 per group. f The timeline of the miR146a-5p-treated CIA mice experiment. g The mean arthritis index scores of mice. Statistical significance was conducted by ANOVA of repeated measurement. h H&E and toluidine blue staining of the knee joints of the mice. Semiquantitative scores (i) for synovial infiltration, synovial hyperplasia, cartilage damage, and bone damage were assessed. j CTGF level in mice synovial fluid was determined by ELISA. n = 10 per group. CIA + NC, CIA mice treated with miRNA-146a-5p-agomir negative control; CIA + miR146a-5p-agomir, CIA mice treated with miR146a-5p-agomir. All data were represented as the mean ± SD. Student’s t test was used to evaluate the statistical significance