| Project/Area Number |
20591278
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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 University of Tokushima, 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) |
KONDO Shuji 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 助教 (00380080)
ROKUTAN Kazuhito 徳島大学, 大学院・ヘルスバイオサイエンス研究部, 教授 (10230898)
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| Project Period (FY) |
2008 – 2010
|
| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2010: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
Fiscal Year 2009: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2008: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 小児腎・泌尿器学 / メサンギウム細胞 / ポドサイト / ボウマン嚢上皮細胞 / 半月体 / 活性酸素 / NAD(P)Hオキシダーゼ / 腎炎進行 / 腎不全 / ボウマン襄上皮細胞 |
|---|
| Research Abstract |
The role of reactive oxygen species for cell phenotypic changes was investigated in glomerulonephritis (GN). Increased ROS production was observed in crescents of GN. The increased ROS production was associated with enhanced Nox2 (an NADPH component) expression and parietal epithelial cell proliferation. We also observed the expressions of angiotensin II and its receptor. In addition, cultured glomerular cells stimulated with angiotensin II and H2O2 showed the enhanced phosphorylation of Erk5, a ROS-related MAPK family. Inhibition with siRNA showed that ROS-MAP kinase signaling pathway might enhance cell potential to survive, and thereby play a role in progression of glomerulonephritis.
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