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Podocyte Loss in Aging OVE26 Diabetic Mice
Author(s) -
Teiken Jennifer M.,
Audettey Janice L.,
Laturnus Donna I.,
Zheng Shirong,
Epstein Paul N.,
Carlson Edward C.
Publication year - 2008
Publication title -
the anatomical record: advances in integrative anatomy and evolutionary biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.678
H-Index - 62
eISSN - 1932-8494
pISSN - 1932-8486
DOI - 10.1002/ar.20625
Subject(s) - podocyte , microbiology and biotechnology , medicine , biology , proteinuria , kidney
Abstract Recent studies show that podocyte nuclear density (N V ) and numbers of renal podocytes per glomerulus (N) are altered in experimental and spontaneous diabetes mellitus. N V and N are generally reduced, and it has been hypothesized that these morphological changes may relate to the loss of glomerular permselectivity in diabetic nephropathy (DN). In the current study, OVE26 transgenic diabetic mice and age‐matched (FVB) controls (60, 150, or 450 days) were fixed by vascular perfusion and renal cortical tissues were prepared for morphometric analyses. ImageJ software and point counting analyses were carried out on light and transmission electron micrographs to determine glomerular volume (V G ), N V , and N. As expected, mean V G in OVE26 mice increased substantially (∼134%) over the course of the study and was significantly increased over FVB mice at all ages. At 60 days, N V and N were not statistically distinguishable in OVE26 and control mice, while at 150 days, N V was significantly reduced in diabetics but not N. In 450‐day‐old OVE26 animals, however, N V and N were both significantly decreased (∼231% and ∼99%, respectively) relative to age‐matched FVB mice. These data suggest that in the OVE26 model of diabetes, significant podocyte loss occurs relatively late in the course of the disease. Moreover, it seems possible that these podocytic changes could play a role in sustaining the increased permeability of the blood–urine barrier in the later stages of diabetic renal decompensation. Anat Rec, 291:114–121, 2007. © 2007 Wiley‐Liss, Inc.