Figure 4

HDAC4 inhibits Runx2 and MMP-13 expression in human OA chondrocytes. (A) Human OA chondrocyte phenotype was confirmed by immunocytochemistry. The cells were positive for type II, but not for type I collagen. (B) Transfection efficiency of HDAC4 in OA chondrocytes was validated by western blotting. (C) Real-time PCR results indicated that overexpression of HDAC4 downregulated Runx2. The experiments were performed in triplicate. Data are presented as means ± SD. (D) HDAC4 inhibited Runx2 promoter activity in the human chondrocyte cell line (C28/12) in a dose-dependent manner. Conversely, inhibition of HDAC by TSA drug enhanced Runx2 promoter activity in a dose-dependent manner. ^* = P <0.05 versus control OA culture; # = P <0.05 versus the group of Runx2 promoter transfection. (E) HDAC4 inhibited MMP-13 promoter activity in the human chondrocyte cell line (C28/12) in a dose-dependent manner. Conversely, inhibition of HDAC by TSA drug enhanced MMP-13 promoter activity in a dose-dependent manner. All transfections were performed in triplicate. ^* = P <0.05 versus control OA culture; # = P <0.05 versus the group of Runx2 promoter transfection. Data are presented as means ± SD. Values represent the mean ± SD from three independent experiments. HDAC4, histone deacetylase 4; MMP, matrix metalloprotease; OA, osteoarthritis; Runx2, runt-related transcription factor-2; SD, standard deviation; TSA, trichostatin A.