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. 2016 Mar 10;49(2):207–218. doi: 10.1111/cpr.12246

Figure 4.

Figure 4

miR‐30a functions during chondrocyte extracellular matrix (ECM) degradation occured through regulation of Sox9. Chondrocytes were cotransfected with miR‐Scr or miR‐30a mimic together with Sox9 full‐length vector (Sox9 expression vector containing both UTR and CDS regions) or Sox9 CDS vector (Sox9 expression vector containing only CDS region, no UTR). The expression of Sox9 mRNA (a) and protein (b) was analyzed by real‐time PCR and western blotting, and the analysis was performed using images of three independent experiments, respectively. Data were normalized to β‐actin. Data were expressed as mean ± SD of three independent experiments. *P < 0.05 versus miR‐Scr + Sox9 full length. Chondrocytes were first transfected with miR‐Scr or miR‐30a inhibitor, and then transfected with either siRNA against Sox9 (siSox9) or scrambled siRNA (siScr). (c) The protein level of Sox9 was analyzed by western blotting. Data were normalized to β‐actin. (d) The sGAG content in the cell suspension was assessed by the dimethylmethylene blue assay. Data were normalized by total protein content in the cell lysate in each group. (e) Col II expression of transfected chondrocytes was assessed by immunofluorescence staining. Scale bars: 50 μm. Data were expressed as mean ± SD of three independent experiments. *P < 0.05 versus miR‐Scr + siScr.