2013 Fiscal Year Final Research Report
A study of mechanisms underlying M3 muscarinic agonist-induced trafficking of AQP5 to nuclei, functions of AQP5 located in nuclear membrane and a development of a drug for age-dependent xerostomia
| Project/Area Number |
23592738
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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 |
Functional basic dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ISHIKAWA Yasuko 徳島大学, ヘルスバイオサイエンス研究部, 准教授 (40144985)
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| Co-Investigator(Kenkyū-buntansha) |
SHONO Masayuki 徳島大学, 大学院ヘルスバイオサイエンス研究部, 技術職員 (60380101)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 水チャネル / アクアポリン-5 / 唾液腺 / 耳下腺 / 細胞核 / 脂質ラフト / 国際情報交換 |
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| Research Abstract |
Activation of M3 muscarinic acetylcholine receptor (mAChR) or alpha 1 adrenoceeptor induces the increase in the amount of aquaporin-5 (AQP) in nuclear membrane and apical plasma membrane of rat parotid glands. We investigated the mechanisms underlying cevimeline (mAChR agonist)-induced trafficking of AQP5 to nuclei. Co-immunoprecipitation of AQP5 and Rab5 was detected in nuclear membrane 3 min after cevimeline-injection. We visualized the distribution of AQP5 and Rab5 in parotid nuclei in response to cevimeline. AQP5 was increased in 1% Triton X-soluble- and -insoluble-nuclear membrane fractions 3 min after cevimeline-injection. Very few AQP5 of nuclear membrane were floated in sucrose density gradient. Under control conditions, the diameter of nuclei was 5.5 micro m. The diameter was decreased to 3.5 micro m 3 min after cevimeline treatment. Administration of artificial saliva (patent no. 2013-022555) prevented age-dependent decreases of AQP5 trafficking to nuclei.
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