| Project/Area Number |
13470393
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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 |
Functional basic dentistry
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| Research Institution | The University of Tokushima |
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Principal Investigator |
ISHIKAWA Yasuko The University of Tokushima, School of Dentistry, Associate Professor, 歯学部, 助教授 (40144985)
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| Co-Investigator(Kenkyū-buntansha) |
YUAN Zhenfang The University of Tokushima, School of Dentistry, Assistant Researcher, 歯学部, 助手 (80346600)
IIDA Hirokazu The University of Tokushima, School of Dentistry, Assistant Researcher, 歯学部, 助手 (10335797)
マーリック ウォーテック・ダニエル 徳島大学, 歯学部, 助手 (00335803)
石田 甫 徳島大学, 歯学部, 教授 (70028364)
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| Project Period (FY) |
2001 – 2003
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| Project Status |
Completed (Fiscal Year 2003)
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| Budget Amount *help |
¥14,400,000 (Direct Cost: ¥14,400,000)
Fiscal Year 2003: ¥2,300,000 (Direct Cost: ¥2,300,000)
Fiscal Year 2002: ¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2001: ¥9,400,000 (Direct Cost: ¥9,400,000)
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| Keywords | Water channel / Aquaporin-5 / Salivary glands / Diabetes / Xerostomia / Lipid rafts / Apical membrane / Cevimeline / SNI-2011 / アクアポリン-5 / アクアポリン-8 / M3ムスカリン受容体 / 唾液分泌不全 / チアゾリジン系薬物 |
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| Research Abstract |
Parotid secretory response to the activation of M3-muscarinic acetylcholine receptors (mAChRs) is reduced in streptozotocin.-induced diabetic (STZ) rats. In this research eve investigated the mechanisms involved in the decreased secretory response in coupled with the alteration of the distribution of aquaporin-5 (AQP5) water channel. Parotid slices from Wister rats gived STZ were incubated with or without mAChR agonists or other agents. Cevimeline hydrochloride (SNI-2011) increased AQPS levels in apical plasma membrane by 3-fold in parotid glands in normal rats, but by 0.8-fold in those of STZ rats. SNI-2011 increases AQP5 levels in basolateral membrane in STZ rats. Although mRNA of AQP5 was increased, the amount of AQP5 in parotid homogenate or lipid rafts was decreased in STZ rats. Both the quantities and affinity of mAChRs were decreased, but the amount of Gq proteins were not changed in STZ rats compared with ncontrol rats. In conclusion, mAChR agonists did not induce the increase in the amount of AQP5 in the apical plasma membrane of parotid glands from STZ rats because of the ~~ defect of translocation of AQP5 from rafts to the apical plasma membrane
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