| Project/Area Number |
07044298
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| Research Category |
Grant-in-Aid for international Scientific Research
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| Allocation Type | Single-year Grants |
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| Section | Joint Research |
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| Research Institution | Okazaki Research Institutes, National Institute for Physiological Sciences |
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Principal Investigator |
MURAKAMI Masataka National Institute for Physiological Sciences, Associate Professor, 生理学研究所, 助教授 (10104275)
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| Co-Investigator(Kenkyū-buntansha) |
FOSKETT J.Kevin University of Toronto School of Medicine (1995), 医学部(平成7年度のみ分担), 助教授
RIVA Alessandro University of Cagliari Faculty of Medicine, 医学部, 教授
STEWARD Martin C Manchester University School of Physiological Sciences (1996), 生理科学部(平成8年度のみ分担), 助教授
SOLTOFF Stephen P Harvard Medical School (1996), 医学部(平成8年度のみ分担), 助教授
TURNER R.James National Institute of Health, 主幹
DISSING Steen Copenhagen University School of Medicine, 医学部, 助教授
YOUNG John A Sydney University Faculty of Medicine, 医学部, 教授
SEGAWA Akihisa Kitasato University School of Medicine, 医学部, 講師 (50154638)
ISHIKAWA Toru National Institute for Physiological Sciences, 生理学研究所, 助手 (70249960)
SEO Yoshiteru Kyoto Prefectural University of Medicine, 医学部, 講師 (90179317)
SUGIYA Hiroshi Nihon University School of Dentistry at Matsudo, 松戸歯学部, 助教授 (20050114)
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| Project Period (FY) |
1995 – 1996
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| Project Status |
Completed (Fiscal Year 1996)
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| Budget Amount *help |
¥11,800,000 (Direct Cost: ¥11,800,000)
Fiscal Year 1996: ¥5,900,000 (Direct Cost: ¥5,900,000)
Fiscal Year 1995: ¥5,900,000 (Direct Cost: ¥5,900,000)
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| Keywords | fluid secretion / electrolyte secretion / cotransporter / antiporter / ion channel / salivary glands / intracellular messenger / energy supply |
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| Research Abstract |
The project aims to study a co-operative mechanism of the transporter proteins (channel, cotransport, antiport & pumps) to produce a macroscopic secretion (concerted mechanism) in the exocrine acinar cells. The project focuses on transport ability, energy supply and its control of transporter proteins in the salivary gland. Collaborative laboratories, using different specialized techniques, measured water & electrolyte movements across cell membranes and intracellular information system in the isolated cells and the vascularly perfused whole gland. NIPS group developed a technique to isolate and perfuse the parotid gland. They measured fluid secretion and oxygen consumption simultaneously, and assessed contribution of Na-dependent transporters to organized secretion. Manchester/Okazaki team measured cell volume change in the whole gland and isolated cells using pulse gradient NMR and fluorometry. They found positive relationship between intracellular Cl and cell volume. Matsudo team fo
… More
und an activity of NOS involving cGMP accumulation in the rabbit parotid gland. They also identified VAMP-2 as a exocytosis-related protein in the vesicle membrane. Copenhagen team measured inositol compounds along the time course of secretion, and found that activation of purinergic receptor inhibit mobilization of IP3 by substance P.NIPS/Harvard team supported experimentally by observation that ATP inhibits fluid secretion by ACh. Harverd team found that CCh and substance P caused phosphorylation of PKC delta as early event, then MAP kinase was activated. Sydney group examined mechanism of ductal K secretion and Na reabsorption. They concluded no contribution of Na/K/2Cl cotransport for ductal K secretion in the mouse, and found involvement of G-protein on NaCl reabsorption in the duct. NIH group examined activation mechanism of Na/K/2Cl cotransporter at molecular level, and found a possible role of cotransporter to excrete ammonium physiologically from saliva. Kitasato/Cagliari team observed 3D structure of intercellular path and exocytosis, and found functional difference in the exocytosis-endocytosis coupling via microfilament between CCh and isoproterenol stimulation. The collaboration allowed to use the same preparation technique of the materials and quite different measurement techniques used by each laboratories, so substantial synergetic results was produced. Less
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