Figure 1.

Glomerular DAF downregulation promotes murine ADR-induced FSGS through a complement-mediated mechanism. (A–F) Representative pictures and data quantification of glomerular (A–C) DAF and (D–F) C3b staining of male WT BALB/c mice treated with vehicle or ADR (10 mg/kg, i.v.). Background staining for C3b is present in the periphery of all glomeruli, with higher intraglomerular C3b staining (arrows) in the ADR-treated animals. DAF and C3b glomerular fluorescence intensity was quantified relative to isotype using ImageJ software. At least 30 glomeruli per mouse from two animals were included in the analysis. Each dot represents a glomerulus. (G and H) Urinary A/C at weekly intervals (G) and representative renal histological (PAS stain) lesions (H) of male WT (n = 8) or DAF^−/− (n = 9) BALB/c mice sacrificed at 5 wk after ADR injection (10 mg/kg, i.v.). (I) Urinary A/C at weekly intervals of female WT (n = 5) or DAF^−/− (n = 4) BALB/c mice sacrificed at 5 wk after ADR injection (10 mg/kg, i.v.). (J–M) Urinary A/C at weekly intervals (J) and representative renal histological (PAS) lesions (K) with data quantification (L and M) of male WT (n = 18), DAF^−/− (n = 13), or DAF^−/−C3^−/− (n = 4) B6 mice sacrificed at 5 wk after ADR injection (20 mg/kg, i.v.). All experimental data were verified in at least three independent experiments. *P < 0.05 versus WT at the same time point. n.s., not significant. Scale bars: 50 µm. Error bars are SEM.