| Project/Area Number |
21790150
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Medical pharmacy
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| Research Institution | Hiroshima University |
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Principal Investigator |
NAGAI Junya 広島大学, 大学院・医歯薬学総合研究科, 准教授 (20301301)
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| Project Period (FY) |
2009 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 抗体(IgG) / レセプター / エンドサイトーシス / IgG / FcRn / 腎障害 / メガリン / キュビリン / エンドサイトーイス / 抗体医薬 |
|---|
| Research Abstract |
In this study, we analyzed the pharmacokinetics of IgG and FcRn expression under normal and disease conditions. In addition, the transport mechanisms of IgG in cultured intestine and kidney epithelial cells were investigated. In rats with CDDP-induced nephrotoxicity, there were no changes in the plasma half life of FITC-IgG and renal FcRn mRNA expression when compared to control rats. On the other hand, renal accumulation of FITC-IgG in rats with CDDP-induced nephrotoxicity was significantly higher than that in control rats. Furthermore, we found that the uptakes of FITC-IgG by human intestinal Caco-2 cells and opossum kidney OK cells are due to FcRn-mediated and megalin/cubilin-mediated endocytosis, respectively.
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