| Project/Area Number |
09671866
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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 |
Morphological basic dentistry
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| Research Institution | Kitasato University |
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Principal Investigator |
SEGAWA Akihisa Kitasato Univ. School of Medicine, Assistant Professor, 医学部, 講師 (50154638)
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| Project Period (FY) |
1997 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 1999: ¥1,100,000 (Direct Cost: ¥1,100,000)
Fiscal Year 1998: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 1997: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | Salivary glands / exocytosis / endocytosis / calcium / IPィイD23ィエD2 receptor |
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| Research Abstract |
This research project is aimed to clarify the molecular mechanisms involved in exocytosis-endocytosis coupling in salivary glands by morphological/functional/biochemical approaches. This year, analyses were performed on whole gland perfusion system, calcium signaling and parotid glands in l3-galactosidase knock-out mice.
1) Whole gland perfusion: Isolated whole parotid glands of rats were perfused arterially with isoproterenol (β-agonist) or carbachol (muscarinic agonist), and secreted saliva and tissues were collected sequentially; β-stimulation evoked exocytosis following which the fused granule membranes were removed one by one. Muscarinic stimulation inhibited this removal process. Since muscarinic stimulation causes fluid secretion but β-stimulation does not, it is suggested that membrane retrieval process plays significant roles in regulation of fluid secretion.
2) Calcium signaling: High speed cofocal microscopy of living parotid glands showed the synchronized response in acini and the non-synchronized response in ducts. Gap junction was detected between acinar cells but not duct cells. Acini are likely to function as a syncitium.
3) β-galactosidase knock-out mice: β-galactosidase is involved in the lysosomal degradation of membrane components. Parotid acinar cells in mice deficient in this enzyme revealed vacuolar profiles in the cytoplasm. Electron microscopic observation demonstrated that the vacuoles appeared in the RER region. Unexpectedly, this enzyme is suggested to play roles in the biosynthetic processes rather than the degradation.
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