| Project/Area Number |
16591035
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Pediatrics
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| Research Institution | The University of Tokushima |
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Principal Investigator |
KAGAMI Shoji The Univ. of Tokushima, Institute of Health Biosciences, Professor, 大学院・ヘルスバイオサイエンス研究部, 教授 (00224337)
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| Co-Investigator(Kenkyū-buntansha) |
URUSHIHARA Maki The Univ. of Tokushima, Institute of Health Biosciences, Assistant Professor, 大学院・ヘルスバイオサイエンス研究部, 助手 (50403689)
黒田 泰弘 徳島大学, 副学長 (20035471)
吉栖 正典 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 講師 (60294667)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2005: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | ILK / Integrin / Parietal epithelial cell / Podocyte / Mesangial cell / Crescent / Sclerosis / Renal failure |
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| Research Abstract |
In order to clarify the role of ILK in progressive glomerulonephritis(GN), we investigated the expression of ILK in experimental GN (anti-Thy-1 GN and WKY masugi GN models) and function of ILK by using cultured cells. Glomerular and crescent ILK expression was increased in parallel with cell proliferation and matrix accumulation during the course of GN. Cell proliferation and collagen contraction assays revealed that ILK expression and activity play an important role in cell proliferation, cell survival and matrix remodeling in cultured glomerular mesangial cells and parietal epithelial cell. Study with dominant negative ILK vector showed that ILK mediated signal pathways necessary for pathological ECM remodeling seen in progressive GN and crescent formation. These results indicate that ILK play a critical role in pathological ECM remodeling in progressive GN. Further study is required for development of pharmacological tool to inhibit ILK activity involved in progression of GN in human.
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