Fig. 5
Silencing miR-92a prevents kidney injury in a mouse model of nephrotoxic nephritis. a Study design of the in vivo preventative antagomir experiment. b RT-qPCR analysis of the relative abundance of miR-92ain freshly isolated glomeruli from normal mice (control), NTS-challenged mice (NTN), NTS-challenged mice treated with anti-miR-control (NTN + anti-miR-ctrl) and NTS-challenged mice treated with anti-miR-92a (NTN + anti-miR-92a) after 10 days. All values are normalized to U6snRNA and are relative to control. Values are means ± s.e.m. (n = 4 per group). *p < 0.05 vs. control, # p < 0.05 vs. NTN alone. c Representative photomicrographs of p57 staining (scale bars, 10 µm), Masson trichrome- (scale bars, 20 µm), silver-stained kidney sections (scale bars, 10 µm) and transmission electron microscopy (scale bars, 0.5 µm) from groups of mice described in a. d Quantification of p57Kip2-positive cells per glomerular section in mice described in a. e Proportion of glomerular crescents in kidney sections, f albuminuria, and g blood urea nitrogen concentrations in mice as described in a. Values are means ± s.e.m. (n = 4 per group). *p < 0.05 vs. control, # p < 0.05 vs. NTN alone. Statistical analysis: Kruskal–Wallis one-way analysis of variance followed by Dunn’s multiple comparaison test
