Fig. 10: SMAD2/3-deficiency abrogates SIRT2 knockout mediated kidney injury.
From: SIRT2 alleviated renal fibrosis by deacetylating SMAD2 and SMAD3 in renal tubular epithelial cells
AAV-Ctrl or AAV-Ggt (gamma-glutamyltransferase 1)-shSmad2/3 was injected into bilateral kidneys of mice in situ at three independent points. After 2-week transfection, mice received UUO surgery, and the contralateral kidneys were used as control. a Western blot analysis of SMAD2, SMAD3, SIRT2 and β-actin in the kidneys from mice at day 10 post-surgery, with quantitative results shown in the right panel, and β-actin used as the loading control (n = 6). b Representative images of SIRT2 immunohistochemical staining in the kidney sections. c–e Representative images of Sirius red and Masson’s trichrome staining were shown (c), and the collagen deposition (c for Sirius red staining and (d) for Masson’s trichrome staining) was quantified in the kidney sections in 3 fields per mice at ×100 magnification (n = 6). f Representative images of E-cadherin immunofluorescence staining were shown in the kidney from mice at day 10 post-surgery. g The mRNA level of Col1a1, α-SMA, Col1a2, and Serpine1 (n = 6). h Western blot analysis of COL3A1, FN1, CTGF, and β-actin in the kidneys from mice at day 10 post-surgery, with quantitative results shown in the right panel, and β-actin used as the loading control (n = 6). For all panels, data are presented as mean ± SD. *P < 0.05, **P < 0.01, ***P < 0.001 by one-way ANOVA with a Bonferroni correction test.
