Signal transduction of intestinal epithelial cells involved in absorption of botulinum toxin.
| Project/Area Number |
24580432
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Basic veterinary science/Basic zootechnical science
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| Research Institution | Tokyo University of Agriculture |
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Principal Investigator |
NIWA Koichi 東京農業大学, 生物産業学部, 教授 (20301012)
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| Co-Investigator(Renkei-kenkyūsha) |
WATANABE Toshihiro 東京農業大学, 生物産業学部, 教授 (80175695)
SAGANE Yoshimasa 東京農業大学, 生物産業学部, 教授 (00624660)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2013: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2012: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
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| Keywords | ボツリヌス毒素複合体 / 家畜ボツリヌス症 / 小腸上皮細胞 / エンドサイトーシス / 透過性 / MAPキナーゼ / 腸管吸収 / ボツリヌス毒素 / 細胞内シグナル / トランスサイトーシス |
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| Outline of Final Research Achievements |
To clarify the mechanisms of absorption of Clostridium botulinum toxin complex (TC) from intestine, cellular signaling and changes in paracellular permeability elicited by TC were examined. An addition of TC caused an increase in paracellular permeability of rat intestinal epithelial IEC-6 cells cultured on a porous membrane of Transwell. TC also activated extracellular signal-regulated kinase (ERK) and p38, members of MAP kinases. The permeability increase induced by TC was abrogated by the p38 inhibitor SB203580. These results indicate that L-TC increases paracellular permeability by activating p38. Because it was observed that TC translocates via transcytosis in experiments with confocal microscopy, we conclude that TC translocates intestinal epithelial cell layers via both intracellular and transcellular pathways.
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Report
(4 results)
Research Products
(7 results)
