| Project/Area Number |
21592375
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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 |
Functional basic dentistry
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| Research Institution | Nihon University |
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Principal Investigator |
SUGIYA Hiroshi 日本大学, 生物資源科学部, 教授 (20050114)
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| Co-Investigator(Renkei-kenkyūsha) |
NARITA Takanori 日本大学, 生物資源科学部, 助教 (70453884)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 顎下腺 / 水分泌 / 傍細胞輸送 / カルシウムイオン / タイト結合 / 翻訳後修飾 / ニューロキニンA / IGF-I / ピロカルピン / 細胞内カルシウム / クローディン / PI3キナーゼ |
|---|
| Research Abstract |
The relationship between neurokinin A-or pilocarpine-provoked salivary fluid secretion and paracellular transport by using Lucifer Yellow was investigated in perfused rat submandibular gland. Salivary fluid secretion provoked by neurokinin A-or pilocarpine was dependent on the increase in intracellular Ca^<2+> concentrations, which was linked to Lucifer Yellow secretion. These results suggest that Ca^<2+>-dependent phosphorylation and/or dephosphorylation appears to contribute to the paracellular transport. On the other hand, expression and localization of tight junction proteins was induced by insulin-like growth factor I(IGF-I) in cultured rat submandibular gland cells, suggesting that IGF-I contributes to maintenance of the paracellular pathway system in salivary gland. Since the IGF-I effect was inhibited by PI3-kinase inhibitors, phosphorylation by PI3-kinase appears to contribute to the effect of IGF-I.
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