Fig. 7
An association of CLU deficiency with more renal fibrosis (tubulointerstitial fibrosis, glomerulopathy and vascular fibrosis) after 30 days of IRI. The sections of CLU KO and WT kidneys, harvested after 30 days of IRI, were stained with MT. a Typical microscopic views of kidney sections in each group (KO: CLU KO kidneys; WT: WT kidneys), showing blue stain of collagen accumulation in the tubulointerstitial area, inside the glomerulus and interlobular arterial wall, and in the perivascular space. G: glomerulus; PT: proximal convoluted tubule; IA: interlobular artery; IF: interstitial fibrosis. b The extent of tubulointerstitial fibrosis was semi-quantitatively scored in at least 20 randomly selected views in two separate sections of each kidney and was presented in average per view. Data are presented as mean ± SD of each group. KO group vs. WT control: P < 0.0001 (two-tailed t-test, n = 8). c The percentage of affected glomeruli (glomerulopathy), including glomerulosclerosis (focal and seqmental sclerosis) and glomerular hypertrophy, was counted in two separate sections of each kidney, and the range of 180 to 250 glomeruli of each kidney was examined. Data are presented as mean ± SD of each group. KO group vs. WT control: P = 0.0300 (one-tailed t-test, n = 8). d The percentage of affected interlobular arterioles or arteries, determined by the presence of the fibrous intima, was counted in two separate sections of each kidney, and the range of 10 to 20 interlobular arteries or arterioles of each kidney was examined. Data are presented as mean ± SD of each group. KO group vs. WT control: P = 0.0144 (two-tailed t-test, n = 8)