The study for mechanism of glomerular epithelial cell decrease in human diabetic nephropathy.
Project/Area Number |
21790822
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Research Category |
Grant-in-Aid for Young Scientists (B)
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Allocation Type | Single-year Grants |
Research Field |
Kidney internal medicine
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Research Institution | Tokai University |
Principal Investigator |
TOYODA Masao Tokai University, 医学部, 講師 (00349383)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2009: ¥3,120,000 (Direct Cost: ¥2,400,000、Indirect Cost: ¥720,000)
|
Keywords | 糖尿病性腎症 / α3β1 / podocin / ZO-1 / 上皮細胞 / Z0-1 |
Research Abstract |
Proteinuria is an important risk factor for the progression of diabetic nephropathy (DN). The podocyte foot processes are connected just above the glomerular basement membrane (GBM) by a special structure known as the slit diaphragm. This structure and the slit diaphragm are important for the maintenance of the glomelurar filter. Podocin, ZO-1 and CD2-AP are major protein in the podocyte slit diaphragm. The expression of these proteins has been studied in kidney tissues of DN. These proteins were quantitated by immunohistochemistry. The relationships between protein expression and clinical parameters were examined. There was an inverse correlation between the percentage of cells positive for podocin protein and extent of proteinuria when all subjects were analyzed. There was a significant correlation between podocin protein expression and urine protein. ZO-1 and CD2-AP proteins were also decreased in DN tissues. Our results suggest that decrease of these podocyte proteins expression might be closely linked to the development and/or progression of human DN.
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Report
(3 results)
Research Products
(3 results)