Fig. 6.
Mice with low EpoR expression in renal tubules had more severe kidney damage and more renal tubulointerstitial fibrosis after acute kidney injury (AKI). AKI was induced in RT-EpoR+/+ mice, RT-EpoR+/− mice, and RT-EpoR−/− mice by bilateral IRI. At predetermined time points, were killed, blood was collected and kidneys were harvested. A: plasma creatinine (PCr). B: Representative micrographs from 4 independent experiments of H&E stain (top) of kidney cortex and OM and kidney injury scores (bottom) obtained in a blinded fashion at days 2 and 7 after IRI. Scale bar = 100 μm. C: renal fibrosis in RT-EpoR+/+ mice, RT-EpoR+/− mice, and RT-EpoR−/− mice. Representative microscopic images from 4 independent experiments of Trichrome stain (left) in kidney sections and renal fibrosis scores (right) obtained in a blinded fashion at day 14 after IRI. Scale bar = 200 μm. Data are expressed as means ± SD (n = 4) from each group, statistical significance was evaluated by one-way ANOVA followed by Student-Newman-Keuls post hoc test, and significance was accepted when *P < 0.05, **P < 0.01, between 2 groups for B and C. D: representative immunoblots from 4 independent experiments for α-SMA and CTGF in the kidney (top) of RT-EpoR+/+ mice, RT-EpoR+/− mice, and RT-EpoR−/− mice at predetermined time points after IRI and a summary of all immunoblots (bottom). Data are expressed as means ± SD from each group, statistical significance was evaluated by one-way ANOVA followed by Student-Newman-Keuls post hoc test, and significance was accepted when *P < 0.05, **P < 0.01 vs. RT-EpoR+/+ mice; #P < 0.05, ##P < 0.01 vs. RT-EpoR+/− mice at same time point for A (n = 6) and D (n = 4).