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. 2013 Sep 5;25(1):33–42. doi: 10.1681/ASN.2012121218

Figure 2.

Figure 2.

Diabetes-mediated Angpt imbalance is ameliorated in mice with Angpt1 repletion. In 8-week-old mice (before treatment with vehicle or doxycycline [DOX]) diabetes led to a decrease in Angpt1 mRNA in isolated glomeruli (D, diabetic; ND, nondiabetic; n=3/group; *P=0.02) (Ai); there was no change in Angpt2 mRNA (Aii). In human podocytes ANGPT1 mRNA was downregulated in high glucose (HG) compared with normal glucose (NG) conditions (Aiii) (n=7–8/group; *P=0.009). In mice with 10 weeks of DOX administration, renal cortical Angpt1 protein was decreased in diabetic mice compared with nondiabetic mice (n=8–11/group; *P=0.002); Angpt1 repletion in diabetic mice resulted in a 20%–30% increase in Angpt1 levels in diabetic mice (n=7–11/group; #P=0.02) (B). X-gal staining of D Pod/Angpt1 mice demonstrated positive expression in glomerular podocytes, indicating the transgene system was working in diabetic mice (B) (X-Gal and eosin staining, magnification x60). Kidney cortical Tie-2 was downregulated in diabetic animals compared with nondiabetic animals (n=7–8/group; *P=0.02) (C); in Pod/Angpt1 DOX diabetic mice, we observed a significant upregulation of Tie-2-P/Tie-2 ratio compared with diabetic control mice (n=7–8/group; #P=0.003) (D). *indicates comparisons between nondiabetic and diabetic state or normal and high glucose conditions; # indicates the comparisons between diabetic states without and with Angpt1 repletion.