Fig. 1
From: Lysosome stress response and mitochondria injury are the earliest detectable alteration in FSGS
Morphological alterations in podocytes after FSGS induction in Nphs2Δpod. (A) Visualisation of the inducible transgenic mouse model and chronological onset of albuminuria, hypertension and proteinuria. (B) Representative PAS-stainings (left) and quantification (right) of the glomerular injury (GI) score in control and Nphs2Δpod mice. Scale bar = 20 µm. n = 4–8 per group with > 40 glomeruli per n. **, P < 0.01 ; ***, P < 0.001. (C) Electron microscopy images of podocytes from control and Nphs2Δpod mice. Red arrow heads point to apical microvilli and yellow arrow heads to enlarged foot processes; red asterisks mark pseudocysts and red hashtags podocyte detachment. Scale bar = 500 nm. (D–H) Quantification of podocyte microvilli (D), pseudocyst formation (E), foot process effacement (F), detachment from the glomerular basement membran (G) and flattened appearance (H). n = 4–5 per group with > 22 podocytes evaluated. *, P < 0.05; **, P < 0.01. (I) Represenative images obtained from glomeruli of each group stained against synaptopodin in green. White arrow heads point to individual podocytes. Scale bar = 20 µm. Higher magnification image is shown below. (J) Quantification of podocyte cell size. The mean of the control is set to 1 and compared to Nphs2Δpod. n = 5–8 per group with > 30 glomeruli evaluated. **, P < 0.01.
