Fig. 3

Pharmacological inhibition of DDR1 activation protects animals against NTS-induced crescentic glomerulonephritis. a Quantitative RT-PCR for Ddr1 mRNA on whole kidney lysate of control mice (Control) and mice injected with nephrotoxic serum and treated with vehicle (vehicle). b Representative Ddr1 in situ hybridization (ISH) performed on tissue harvested from mice 14 days after NTS injection. * = crescent c representative DDR1 ISH double labelling with alpha smooth muscle actin (Acta2) or EGF-like module-containing mucin-like hormone receptor-like 1 (Emr-1) in control mice (Control) and mice injected with nephrotoxic serum and treated with vehicle (Vehicle). Arrows = cells labeled with Acta2 or Emr-1. d–g Body weight evolution (day 1, 4, 7 and 14) and renal function parameters (e–g blood urea nitrogen (BUN), serum creatinine and proteinuria) measured at sacrifice (day 14). h Representative histopathology with Hematoxylin and Eosin (H&E) and Periodic Acid Schiff staining (PAS) and immunohistochemistry for desmin, CD44, Collagen type IV and Ki67. i Glomerular or tubulo-interstitial (TI) summary scores from semiquantitative histopathologic evaluation on H&E and PAS stained kidney sections respectively. j Morphometry analysis of collagen IV IHC. Statistically significant p value: p < 0.05 = *; p < 0.005 = **. Magnification ×200, scale bar 100 μm