Fig. 5.
hEpoRW/W mice with low EpoR signaling activity had more severe kidney damage induced by IRI. AKI was induced in WT and hEpoRW/W mice by IRI. At predetermined time points, mice were killed, blood was collected and kidneys were harvested. A: plasma creatinine (PCr). Data are expressed as means ± SD (n = 6) from each group, statistical significance was assessed by unpaired Student’s t-test, and significance was accepted when *P < 0.05, **P < 0.01, between 2 groups at same time point. B: histologic kidney damage in WT mice and hEpoRW/W mice. Representative micrographs from 4 independent experiments of hematoxylin and eosin (H&E) stain (top) in 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. Data are expressed as means ± SD (n = 4) from each group and 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. C: renal fibrosis in WT mice and hEpoRW/W mice. Representative micrographs from 4 independent experiments of Trichrome stains (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 assessed by unpaired Student’s t-test, and significance was accepted when *P < 0.05, **P < 0.01, between 2 groups. D: representative immunoblots from 4 independent experiments for α-smooth muscle actin (α-SMA) and connective tissue growth factor (CTGF) in the kidney (top) of WT mice and hEpoRW/W mice at predetermined time points after IRI. Summary of arbitrary units from all immunoblots (bottom). Data are expressed as means ± SD (n = 4) from each group, statistical significance was evaluated by unpaired Student’s t-test, and significance was accepted when *P < 0.05, **P < 0.01, between 2 groups at same time point.