Fig. 7: Systemic administration of WIF1 exacerbates glomerular injury in diabetic mice and fibrosis in UUO mice.

a Development of albuminuria (shown as the fold change in the ratio of albumin to creatinine) in AAV-CTL and AAV-WIF1 treated mice after 12 weeks of the last injection of STZ (n = 10 biologically independent animals, **P < 0.01). b GSI in kidneys from the AAV-CTL and AAV-WIF1 treated mice 12 weeks after the last dose of STZ injection (20 glomeruli per mouse were analyzed, n = 5 biologically independent animals per group, *P < 0.05). c–f Glomerular gene expression of Wt1 (c), Nphs1 (d), Nphs2 (e), and Podxl (f) (n = 7 biologically independent animals, *P < 0.05). g–i Representative immunofluorescence images for NPHS1 (g), NPHS2 (h), and PODXL (i) in kidney sections from the AAV-CTL and AAV-WIF1 treated mice. Scale bar, 20 μm. j–l Kidney gene expression of α-SMA, Col1a1 and Fn (n = 5 biologically independent animals, *P < 0.05, **P < 0.01). m–p Western blotting analysis of α-SMA, COL1A1, and FN in kidneys from the AAV-CTL and AAV-WIF1 treated mice. Densitometry calculations are normalized to β-actin as indicated (n = 4 biologically independent animals, *P < 0.05). q–s Immunofluorescence for α-SMA, COL1A1, and FN in kidney sections from the AAV-CTL and AAV-WIF1 treated mice. Scale bar, 50 μm. t Relative area of fibrosis (%) measured using ImageJ (**P < 0.01). n = 7 biologically independent mice/group from two separate experiments. Data are mean ± SEM. Data are presented as mean values ± SEM. Two-tailed unpaired Student’s t test was used for statistical comparisons (a–f, j–l, n–p, t). Source data are provided as a Source data file.