Fig. 2: Podocyte-specific Cldn5 deletion mice show increased susceptibility to diabetic kidney injury. | Nature Communications

Fig. 2: Podocyte-specific Cldn5 deletion mice show increased susceptibility to diabetic kidney injury.

From: Loss of CLDN5 in podocytes deregulates WIF1 to activate WNT signaling and contributes to kidney disease

Fig. 2

a Double immunostaining of CLDN5 and NPHS2 of kidney sections from control and DN (UNX/STZ) mice 12 weeks after the last injection of STZ. Scale bars, 20 μm. b Double immunostaining of CLDN5 and NPHS2 in kidney sections from control (DB/M) and DN (DB/DB) mice at 24 weeks of age. Scale bars, 20 μm. c Development of albuminuria (shown as the fold change in the ratio of albumin to creatinine) in CTL (WT) and KO (Cldn5 KO) mice after 4, 8, and 12 weeks of the last injection of STZ (n = 11 biologically independent animals, ****P < 0.0001). d–f PAS staining (d), GSI (e), and mesangial area expansion (f) in WT and Cldn5 KO mice 12 weeks after the last dose of STZ injection (20 glomeruli per mouse were analyzed, n = 5 mice per group, **P < 0.01, ****P < 0.0001). Scale bar, 50 μm. g–i TEM images of glomerular capillary loops of WT and Cldn5 KO mice (g) and quantification of GBM thickness (h) and FP number (i) 12 weeks after the last dose of STZ injection (n = 3 biologically independent animals and 20 images per group, ****P < 0.0001). Scale bar, 0.5 μm. j Immunostaining of podocyte injury marker desmin in kidney sections from WT and Cldn5 KO mice 12 weeks after the last STZ injection. Nuclei were visualized by DAPI. Scale bars, 20 μm. k MTS images of whole kidney showing interstitial fibrosis in Cldn5 KO diabetic mice 12 weeks after the last injection of STZ. Scale bars, 200 μm. Data are presented as mean values ± SEM. Two-tailed unpaired Student’s t test was used for statistical comparisons (c, e, f, h, i). Source data are provided as a Source data file.

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