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. 2020 Aug 20;5(16):e140458. doi: 10.1172/jci.insight.140458

Figure 2. Human scleroderma increases promoter accessibilities of JUN and CD47.

Figure 2

(A) ATAC-Seq analysis for JUN and the hedgehog genes Gli1 and Ptch1 in scleroderma fibroblasts (SSCL), scleroderma fibroblasts after JUN knockout (JUN-KO) or under vismodegib, and normal skin fibroblasts. The promoter regions are highlighted with red boxes. n = 2. (B) ATAC-Seq analysis for the immune checkpoints CD47 and PD-L1 and the interleukin IL-6 in scleroderma fibroblasts, scleroderma fibroblasts after JUN knockout or under vismodegib, and normal skin fibroblasts. The promoter regions are highlighted with red boxes. n = 2. (C) Heatmap of differential open chromatin regulatory elements characterized from ATAC-Seq. The color bar shows the relative ATAC-Seq signal (Z score of normalized read counts) as indicated. Samples 1 and 2 in both groups are individual samples. n = 2. (D) Fibrosis-linked genes with a 5-fold decline in promoter accessibility after JUN knockout. n = 2. (E) p-JUN expression in pulmonary fibroblasts and scleroderma fibroblasts on a 70 kPa hydrogel or a regular polystyrene plastic dish. Two-sided t test. **P < 0.01; ***P < 0.001. n = 4. Tukey’s multiple comparison test. Bars represent means with standard deviations.