The study for mechanism of glomerular epithelial cell decrease in human diabetic nephropathy.

Research Project

Project/Area Number	21790822
Research Category	Grant-in-Aid for Young Scientists (B)
Allocation Type	Single-year Grants
Research Field	Kidney internal medicine
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.