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1 Nephrology Division and 2 Gastroenterology and Hepatology Division of the Department of Medicine and 3 Department of Anatomy, Pathology, and Cell Biology, Thomas Jefferson University School of Medicine, Philadelphia, Pennsylvania 19107
The mechanisms
underlying glomerular hypertrophy and hyperfiltration in diabetes
remain unclear. We have previously demonstrated that the cytokine
transforming growth factor-
1 (TGF-1) is increased in early
diabetic kidney disease and TGF-1 inhibits the expression of the
inositol 1,4,5-trisphosphate
(IP3)-gated calcium channel, the
type I IP3 receptor
(IP3R), in mesangial cells. To
test the hypothesis that reduced type I
IP3R may be important in diabetic kidney disease, we evaluated type I
IP3R expression in the kidney of
streptozotocin-induced diabetic rats and mice. Two-week-old diabetic
rats have decreased renal type I
IP3R protein and mRNA levels.
Immunostaining of normal rat kidney demonstrated presence of type I
IP3R in glomerular and vascular
smooth muscle cells, whereas diabetic rats had reduced staining in both
compartments. Reduction of type I
IP3R also occurred in parallel
with renal hypertrophy, increased creatinine clearance, and increased
renal TGF-1 expression in the diabetic rats. Two-week-old diabetic mice also had reduced renal type I
IP3R protein and mRNA expression in association with renal hypertrophy and increased TGF-1 mRNA expression. These findings demonstrate that there is reduced type I
IP3R in glomerular and vascular
smooth muscle cells in the diabetic kidney, which may contribute to the
altered renal vasoregulation and renal hypertrophy of diabetes.
inositol 1,4,5-trisphosphate receptor; diabetic renal hypertrophy; transforming growth factor-; hyperfiltration
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