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. 2020 Oct 6;28(3):1001–1012. doi: 10.1038/s41418-020-00631-9

Fig. 6. Klotho derepression is essential for the antifibrosis function of HDAC3 inhibition.

Fig. 6

Mice receiving siRNA-Control (siCon) or siRNA-Klotho (siKL) were subgrouped into Sham, RGFP966, UUO, and RGFP966-treated UUO (n = 6). a Representative photomicrographs of kidney sections (Masson’s trichrome staining). The dark arrows indicate fibrotic areas. b Quantitation of renal fibrosis in a. The effects of siRNA-Klotho (P1), RGFP966 intervention (P2), and the interaction between siRNA-Klotho and RGFP966 intervention (P3) were indicated. c Western blots. The renal tissues from experimental mice in a were assayed for Klotho, α-SMA, BMP-7, collagen 1 (Colla 1), and d β-catenin (β-cat) and phosphorylated Smad2 (p-Smd2). Two samples from each group were shown. e Quantification of c and d. Data were presented as means ± SEM. *P < 0.05, three-way ANOVA followed by Tukey’s post-hoc test.