Figure 2
From: APOBEC-1 deletion enhances cisplatin-induced acute kidney injury
Deletion of Apobec1 leads to severe cisplatin-induced and ischemia reperfusion-induced AKI. (A) Schematic representation of experimental design for mouse model of AKI. (B) Survival of WT versus KO mice after cisplatin treatments. Data from (B) were analyzed using Kaplan–Meier curves and a log-rank test, n = 18, ***p < 0.0001. (C) Plasma creatinine level at Day 4 post CP injection, one way ANOVA multiple comparison, n = 10, **p < 0.001, ***p < 0.0005 ****p < 0.0001. (D) Schematic representation of experimental design for mouse model of IR. (E) Plasma creatinine level 24 h after IR surgery, one way ANOVA multiple comparison, n = 5 in control and WT AKI groups and n = 6 in KO AKI group, *p < 0.05, **p < 0.01. (F) Plasma KIM-1 level 24 h after IR surgery, one way ANOVA multiple comparison, n = 5 in control and WT AKI groups and n = 6 in KO AKI group, **p < 0.01, ****p < 0.0001. (G) Representative figures of hematoxylin and eosin staining from different groups of CP-AKI mouse model. Renal damage indicators are represented: → : accumulation of protein casts in the renal tubules. & region: tubule swelling. *loss of brush border membrane. #cell debris detachment. (H) Acute kidney injury scores revealed by hematoxylin and eosin staining from different groups of CP-AKI mouse model. (I) Immunoblotting of kidney injury markers KIM-1 and NGAL in total kidney lysate from WT and KO mice treated with CP for 4 days, n = 3 from each group. GAPDH was used as a loading control. Note that cropped blots are displayed, uncropped blots are included in the supplemental information file. Quantification of KIM-1 (J) and NGAL (K) from immunobotting, one way ANOVA multiple comparison, n = 3, **p < 0.01, ***p < 0.0005, ****p < 0.0001.
