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- W2400712563 abstract "The mechanisms underlying glomerular hypertrophy and hyperfiltration in diabetes remain unclear. We have previously demonstrated that the cytokine transforming growth factor-β1 (TGF-β1) is increased in early diabetic kidney disease and TGF-β1 inhibits the expression of the inositol 1,4,5-trisphosphate (IP 3 )-gated calcium channel, the type I IP 3 receptor (IP 3 R), in mesangial cells. To test the hypothesis that reduced type I IP 3 R may be important in diabetic kidney disease, we evaluated type I IP 3 R expression in the kidney of streptozotocin-induced diabetic rats and mice. Two-week-old diabetic rats have decreased renal type I IP 3 R protein and mRNA levels. Immunostaining of normal rat kidney demonstrated presence of type I IP 3 R in glomerular and vascular smooth muscle cells, whereas diabetic rats had reduced staining in both compartments. Reduction of type I IP 3 R also occurred in parallel with renal hypertrophy, increased creatinine clearance, and increased renal TGF-β1 expression in the diabetic rats. Two-week-old diabetic mice also had reduced renal type I IP 3 R protein and mRNA expression in association with renal hypertrophy and increased TGF-β1 mRNA expression. These findings demonstrate that there is reduced type I IP 3 R in glomerular and vascular smooth muscle cells in the diabetic kidney, which may contribute to the altered renal vasoregulation and renal hypertrophy of diabetes." @default.
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- W2400712563 date "1999-01-01" @default.
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- W2400712563 title "Renal type I inositol 1,4,5-trisphosphate receptor is reduced in streptozotocin-induced diabetic rats and mice" @default.
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- W2400712563 doi "https://doi.org/10.1152/ajprenal.1999.276.1.f54" @default.
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