Figure 3: LCN2 deficiency protects from proteinuria-induced tubular lesions and apoptosis.
From: Endoplasmic reticulum stress drives proteinuria-induced kidney lesions via Lipocalin 2
(a) Renal tubular (periodic acid–Schiff (PAS); scale bar, 100 μm) and (b) glomerular (PAS; scale bar, 50 μm) morphology (upper panels) and quantifications (lower panels) in control (n=6), WT1+/mutXLcn2+/+ (n=10) and WT1+/mutXLcn2−/− (n=10) mice, 6 weeks after birth. (c) Quantification of urine albumin/creatinine ratio in control (n=6), WT1+/mutXLcn2+/+ (n=5) and WT1+/mutXLcn2−/− (n=10) mice at the time of killing. (d) Survival curve of WT1+/mutXLcn2+/+ (n=37) and WT1+/mutXLcn2−/− (n=24) mice. (e) Tubular cell apoptosis evaluated using TUNEL (upper panel; scale bar, 100 μm) and quantification (lower panels) in control, WT1+/mutXLcn2+/+ and WT1+/mutXLcn2−/− mice (n=6 per group). (f) Apoptosis measurement by annexin V staining in scramble and Lcn2 sh-RNA expressing mIMCD-3 cells exposed to albumin for 24 h (n=3). (g) ROS abundance in scramble and LCN2 shRNA expressing mIMCD-3 cells exposed to albumin for 24 h (n=4). (h) Apoptosis measurement by annexin V staining in Lcn2+/+ or Lcn2−/− MEFs exposed to 10% albumin for 24 h in the presence of either NAC or the vehicle (PBS) (n=3). Data are mean±s.e.m. Statistical analysis: one way analysis of variance followed by Tukey–Kramer test; *P<0.05, **P<0.01, ***P<0.001 versus control; #P<0.05, ###P<0.001 versus Lcn2+/+; log rank test (d) P<0.05.
