The cross-talk and secretion in intracellular signaling in parotid glands
| Project/Area Number |
05671546
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Functional basic dentistry
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| Research Institution | Health Sciences University of Hokkaido, School of Dentistry |
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Principal Investigator |
TOJYO Yosuke Health Sciences University of Hokkaido, School of Dentistry, Associate Professor, 歯学部, 助教授 (90111731)
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| Co-Investigator(Kenkyū-buntansha) |
MATSUI Satoko Health Sciences University of Hokkaido, School of Dentistry, Reserch Associate, 歯学部, 助手 (30190391)
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| Project Period (FY) |
1993 – 1994
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| Project Status |
Completed (Fiscal Year 1994)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1994: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1993: ¥1,300,000 (Direct Cost: ¥1,300,000)
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| Keywords | Parotid gland / Intracellular signaling / Cross-talk / Pottassium release / Intracellular calcium / Protein kinase C / muscarinic receptor / Purinergic receptor / 細胞内カルシウムイオン / 細胞外ATP / アミラーゼ分泌 / ホスファターゼ阻害薬 / サイフリックAMP / 唾液腺 / 耳下腺細胞 / ホルボールエステル / スタウロスポリン |
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| Research Abstract |
1) Treatment with the intracellular Ca^<2+> antagonist TMB-8 or the intracellular Ca^<2+> chelator BAPTA-AM strongly suppressed the carbachol (CCh)-induced K^+ release from rat parotid acini. Combined addition of ionomycin anf thapsigargin caused a rapid increas in [Ca^<2+>] and resulted in a marked release of K^+. PMA did not potenciate the CCh-induced K^+ release. The results indicate that the K^+ release is prrimarily mediated by a rapid increase in [Ca^<2+>]_1 but is not associated with activation of proteon kinase C.
2) PMA attenuated the CCh-induced increase in [Ca^<2+>]_1 through inhibition of phosphoinositide hydrolysis. Activation of protein kinase C may play a role in negative-feedback control of the muscarinic pathway in rat parotid acinar cells.
3) Staurosporine enhanced Ca^<2+> entry induced by depletion of intracellular Ca^<2+> stores in rat parotid acinar cells. By contrast, the phosphatase inhibitors suppressed the Ca^<2+> entry. The results suggest that phosphorylation-dephosphorylation mechanism is involeved in the regulation of the capacitative Ca^<2+> entry.
4) The increase in [Ca^<2+>]_1 induced through muscarinic receptors was inhibited by external ATP.This result suggests that is a cross-talk mechanism between muscarinic receptors and purinergic ones in rat parotid acinar cells.
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Report
(3 results)
Research Products
(10 results)
