| Project/Area Number |
20390044
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Medical pharmacy
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| Research Institution | Nagoya University (2009-2010)
Tohoku University (2008) |
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Principal Investigator |
NAKAJIMA Akira 名古屋大学, 医学系研究科, 特任講師 (20419237)
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| Co-Investigator(Kenkyū-buntansha) |
MANO Nariyasu 東北大学, 病院, 教授 (50323035)
TOMIOKA Yoshihisa 東北大学, 大学院・薬学研究科, 教授 (00282062)
YAMAGUCHI Hiroaki 東北大学, 病院, 助教 (80400373)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥19,630,000 (Direct Cost: ¥15,100,000、Indirect Cost: ¥4,530,000)
Fiscal Year 2010: ¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2009: ¥5,460,000 (Direct Cost: ¥4,200,000、Indirect Cost: ¥1,260,000)
Fiscal Year 2008: ¥9,750,000 (Direct Cost: ¥7,500,000、Indirect Cost: ¥2,250,000)
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| Keywords | トランスポーター / 胆汁酸 / 黒質 / in silico / 黒室 |
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| Research Abstract |
We have focused on a newly discovered human brain-specific transporter SLC10A4, which is specifically localized in the substantia nigra. Over-expression cell of human SLC10A4 was successfully generated using human HepG2 cell. A low SLC10A4-mediated uptake of bile acids, such as chenodeoxycholic acid and ursodeoxycholic acid, was observed in the transformant. The expression of SLC10A4 was investigated in various cultured cells using immunoblot analysis. Finally, human brain-derived TE671(medulloblastoma) cells were found that they had a stable expression of SLC10A4. It was noteworthy finding that the uptake of taurocholic acid was induced by thrombin pretreatment in the TE671 cells and the Km value was higher than that of known sodium taurocholate co-transporting polypeptides, such as ASBT and NTCP. We considered that SLC10A4 was special brain transporter, could be activated and responsible for the uptake of bile acids when blood clotting was occurred following blood vessel damage or tissue injury.
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