Journal: Research
Article Title: Epigenetic Suppression of RASAL1 by HDAC3 and Cofactor YY1 Promotes Fibroblast–Myofibroblast Transition and Renal Fibrosis
doi: 10.34133/research.1073
Figure Lengend Snippet: HDAC3 knockout resists RASAL1 suppression and renal fibrosis in fibrotic mice. (A) Schematic diagram of the construction of fibroblast-specific Hdac3 knockout mice ( Hdac3 fl/fl -Col1a2 -CreER, Hdac3 Fb−/− ). Black arrows indicate the location of genotyping primers. (B) Genotyping of Hdac3 wild-type (WT), Hdac3 fl/fl (top), and conditional Hdac3 Fb−/− mice (bottom). (C) Schematic diagram of the animal experiment design and process. ip, intraperitoneally. (D) Hdac3 fl/fl and Hdac3 Fb−/− mice were subjected to sham or UUO for 7 d or to control or AAI for 14 d, 6 mice per group. Left: Representative photomicrographs of kidney sections stained with Masson’s trichrome from all groups. Right: Representative photomicrographs of kidney sections stained with Sirius Red from all groups. The black arrows indicate collagen-stained fibrotic areas. (E) Quantifications of renal fibrosis stained with Masson’s trichrome and Sirius Red from the experimental mice indicated above. (F) Western blotting. The renal tissue homogenates were assayed for HDAC3, RASAL1, α-SMA, Colla 1, and β-actin, which served as the internal control. Two randomly selected samples from each group were shown. (G) Quantifications of (F). Data were presented as means ± SEM based on 6 renal samples. *P < 0.05, 2-way ANOVA.
Article Snippet: To generate the conditional Hdac3 Fb−/− , Hdac3 fl/fl mice containing 2 loxP sites, one upstream of exon 11 and the other downstream of exon 14 of Hdac3 gene [ ], were bred with transgenic Col1a2 -CreER mice (C001248, Cyagen Biosciences, Suzhou, China).
Techniques: Knock-Out, Control, Staining, Western Blot
