Fig. 1: UTX-dependent reduction in chondrocytic activities. | Cell Death & Disease

Fig. 1: UTX-dependent reduction in chondrocytic activities.

From: Histone H3K27 demethylase UTX compromises articular chondrocyte anabolism and aggravates osteoarthritic degeneration

Fig. 1

Safranin-O staining of macroscopically normal human articular cartilage next to severely osteoarthritic tissue. Quantification of UTX mRNA abundance in both tissues revealed elevated UTX expression in gonarthrotic cartilage (a); scale bar, 200 μm. Strong UTX (b) and H3K27me3 (c) immunostaining in osteoarthritic chondrocytes, next to quantified protein expression from 34 donors; scale bar, 20 μm (low magnification), 10 μm (high magnification). Forced UTX expression increased H3K27me3 levels and reduced Sox9 abundance in articular chondrocytes (d). Utx gain-of-function upregulated H3K27me3 enrichment at the Sox9 promoter (e), but reduced Sox9, Col2a1 and Acan expression (f), respectively, and glycosaminoglycan synthesis (g) quantified by Alcian blue staining; scale bar, 500 μm. Utx knockdown repressed H3K27me3 levels and promoted chondrocytic activity. Cells were transfected with Utx RNAi or cDNA or scramble control for 24 hours. RT-PCR was conducted upon transfection for 24 h. Micromass for Alcian blue staining were incubated for 7 days. Culture experiments were conducted from three to five mice and data are expressed as mean ± standard error; *P < 0.05; **P < 0.001. SC scrambled control.

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