Fig. 2.
Irf8 deletion aggravates renal dysfunction during AKI. Irf8+/+ and Irf8−/− mice were subjected to unilateral ischemic reperfusion (IR) surgery and sacrificed 1 day or 7 days after AKI. The healthy group represents mice that did not undergo IR surgery. (A) Blood urea nitrogen (BUN) levels and serum creatinine (CR) levels (n ≥ 3 per group). (B) Weight loss in the kidneys of the IR group compared to that of the sham group was determined as follows: Delta kidney weight = KWIR – KWcontralateral (n ≥ 3 per group). (C) PAS-stained sections and tubular injury scores were evaluated in high-power fields (n = 4 per group). Scale bar, 100 μm. Red star: cast formation; Blue arrow: cell necrosis. Green arrow: tubular dilation. (D) The upper panel shows images of proximal tubules and distal tubules with immunolabeling for aquaporin-1 (AQP1, red) and Tamm-Horsfall protein-1 (THP-1, green) in the cortex, outer stripe of the outer medulla (OSOM), and inner stripe of the outer medulla (ISOM) (scale bar, 200 μm) from IR kidneys or sham kidneys on day 1 after AKI. Nuclei were counterstained with DAPI (blue). The bottom panel shows magnified IR kidney sections from Irf8+/+ and Irf8−/− mice (scale bar, 100 μm). (E) The mRNA expression of tubular injury markers in the healthy group and AKI-1D group was normalized to 18S rRNA expression (n = 3 per group). Each dot represents one mouse. The data are shown as the mean ± SD. *p < 0.05, **p < 0.01, ***p < 0.001, and ****p < 0.0001. Two-way ANOVA. (For interpretation of the references to color in this figure legend, the reader is referred to the Web version of this article.)