Oudit GY, Liu GC, Zhong J, Basu R, Chow FL, Zhou J, Loibner H, Janzek E, Schuster M, Penninger JM, Herzenberg AM, Kassiri Z, Scholey JW. Human recombinant ACE2 reduces the progression of diabetic nephropathy. Diabetes 2010;59:
In the print version of the article listed above, the third and fourth labels on the top of Figure 2 and the third and fourth labels on the top and bottom of Figure 3 are incorrect. The correct figures appear below. The online version reflects these changes.
Glomerular mesangial expansion and thickening of basement membrane were reduced by treatment with human recombinant ACE2. A–C: Representative light micrographs of periodic acid Schiff–stained kidney sections from each group of mice (magnification ×630) (A) with quantification of the glomerular volume (C) showing glomerular expansion in the diabetic Akita mice and a marked reduction in response to hrACE2. B and D: Transmission electron microscopy of the glomeruli (B) with quantification of the glomerular basement thickness (D) showing increased glomerular basement membrane thickness in the Akita Ins2WT/C96Y mice, which was normalized by treatment with hrACE2. White arrows indicate the glomerular basement membrane. E: Mesangial matrix expansion score showing increased mesangial expansion in diabetic Akita kidneys, which was prevented by hrACE2. n = 5 for all groups. *P < 0.05 compared with all other groups and #P < 0.05 compared with placebo + Ins2WT/WT group using ANOVA with multiple comparison testing. (A high-quality digital representation of this figure is available in the online issue.)
Glomerular mesangial expansion and thickening of basement membrane were reduced by treatment with human recombinant ACE2. A–C: Representative light micrographs of periodic acid Schiff–stained kidney sections from each group of mice (magnification ×630) (A) with quantification of the glomerular volume (C) showing glomerular expansion in the diabetic Akita mice and a marked reduction in response to hrACE2. B and D: Transmission electron microscopy of the glomeruli (B) with quantification of the glomerular basement thickness (D) showing increased glomerular basement membrane thickness in the Akita Ins2WT/C96Y mice, which was normalized by treatment with hrACE2. White arrows indicate the glomerular basement membrane. E: Mesangial matrix expansion score showing increased mesangial expansion in diabetic Akita kidneys, which was prevented by hrACE2. n = 5 for all groups. *P < 0.05 compared with all other groups and #P < 0.05 compared with placebo + Ins2WT/WT group using ANOVA with multiple comparison testing. (A high-quality digital representation of this figure is available in the online issue.)
Increased glomerular expression of α-SMA and collagen III in the diabetic Akita kidneys without evidence of inflammatory changes in response to human recombinant ACE2. A–D: Increased glomerular immunostaining for α-SMA (A) and collagen III (B) in diabetic Akita mice that was quantified based on computer image analysis scores of glomerular immunostaining of α-SMA (C) and collagen III (D). Positive controls are shown as staining in renal blood vessels for α-SMA and from a kidney after 14 days of ureteral obstruction for collagen III. n = 5 for all groups. *P < 0.01 compared with all other groups using ANOVA and multiple comparison testing. E and F: Immunohistochemical-specific staining of neutrophil and macrophage revealed no evidence of inflammation in the diabetic Akita mice without a differential impact with treatment with hrACE2. Positive controls were taken from mouse spleen and lung tissue. Scale bar, 100 μm. (A high-quality digital representation of this figure is available in the online issue.)
Increased glomerular expression of α-SMA and collagen III in the diabetic Akita kidneys without evidence of inflammatory changes in response to human recombinant ACE2. A–D: Increased glomerular immunostaining for α-SMA (A) and collagen III (B) in diabetic Akita mice that was quantified based on computer image analysis scores of glomerular immunostaining of α-SMA (C) and collagen III (D). Positive controls are shown as staining in renal blood vessels for α-SMA and from a kidney after 14 days of ureteral obstruction for collagen III. n = 5 for all groups. *P < 0.01 compared with all other groups using ANOVA and multiple comparison testing. E and F: Immunohistochemical-specific staining of neutrophil and macrophage revealed no evidence of inflammation in the diabetic Akita mice without a differential impact with treatment with hrACE2. Positive controls were taken from mouse spleen and lung tissue. Scale bar, 100 μm. (A high-quality digital representation of this figure is available in the online issue.)
