Rosiglitazone Treatment of Type 2 Diabetic db/db Mice Attenuates Urinary Albumin and Angiotensin Converting Enzyme 2 Excretion
Figure 4
Immunofluorescence of nephrin, ACE2 and ADAM17 after 8 weeks of treatment with rosiglitazone.
(A) Immunofluorescence staining for nephrin in the glomeruli of control, untreated and rosiglitazone treated db/db mice at 20× magnification. Nephrin expression was significantly decreased in db/db mice. After eight weeks of treatment with rosiglitazone there was a significant increase in nephrin expression compared to untreated db/db mice. *p<0.01 Vs control mice. #p<0.05 Vs untreated db/db mice. Each bar represents mean ± SEM of group size (n = 11–18). (B) Immunofluorescence staining for ACE2 in cortical tubules and glomeruli of control, untreated and rosiglitazone treated db/db mice at 20× magnification. White arrows indicate glomeruli. While tubular ACE2 expression was increased, glomerular ACE2 expression was significantly decreased in db/db mice. After eight weeks of treatment with rosiglitazone there was a significant increase in glomerular ACE2 expression while tubular ACE2 expression was unchanged compared to untreated db/db mice. *p<0.001 Vs control mice. #p<0.01 Vs untreated db/db mice. Each bar represents mean ± SEM of group size (n = 11–18). (C) Immunofluorescence staining for ADAM17 in cortical tubules of control, untreated and rosiglitazone treated db/db mice at 20× magnification. (D) Immunofluorescence double staining for ACE2 and ADAM17 in cortical tubules of db/db mice at 60× magnification.