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. 2017 Oct 23;8:1346. doi: 10.3389/fimmu.2017.01346

Figure 8.

Figure 8

Renal pathology in unilateral ureter obstruction (UUO)-treated IL-36α- knockout (KO) mice. (A) Genomic structure of IL-36α. Parts of exon 2 and exon 3 are deleted by CRISPR/Cas9 system to generate IL-36α-KO mice. (B) Immunohistochemistry for IL-36α in the kidneys of wild-type (WT) and IL-36α-KO mice at 48 h after UUO. (C) Indices for renal pathology and function in Sham and UUO groups at 48 h. Median. Box = 25th and 75th percentiles. Bars = min and max values. A significant difference from the Sham group in same genotype is indicated by *(P < 0.05) or **(P < 0.01). A significant difference between WT and IL-36α-KO in UUO group is indicated by †(P < 0.05). n ≥ 7 mice. The ratio of UUO kidney weight (KW) to Cont KW is expressed as KW ratio (UUO/Cont). (D) Renal histopathology at 48 h after UUO. Immunohistochemistry and periodic acid Schiff (PAS) stain. In PAS staining, the dilation of distal tubules (DTs) (circles) was milder in UUO kidneys compared to WT kidneys after UUO. (E) Indices for renal histopathology in Cont kidney and UUO kidney of WT and IL-36α-KO mice. Median. Box = 25th and 75th percentiles. Bars = min and max values. A significant difference from the Sham group in the same genotype is indicated by *(P < 0.05) or **(P < 0.01). A significant difference between WT and IL-36α-KO in UUO group is indicated by ††(P < 0.01) (n ≥ 7 mice).