| Project/Area Number |
03670867
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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 | HIROSHIMA UNIVERSITY |
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Principal Investigator |
DOHI Toshihiro Dept.Pharmacology, Hiroshima University School of Dentistry, Professor, 歯学部, 教授 (00034182)
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| Co-Investigator(Kenkyū-buntansha) |
TSURU Hiromichi Dept.Removable Prosthodontics, Hiroshima University School of Dentistry, Profess, 歯学部, 教授 (90034157)
MORITA Katsuya Dept.Pharmacology, Hiroshima University School of Dentistry, Assistant Professor, 歯学部, 講師 (10116684)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 1992: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1991: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | Submandibular gland / Mucin / Signal transduction / GTP binding protein / IP_3 / Calcium / Cyclic ADP-ribose / Platelet-activating factor / イヌ顎下腺腺房細胞 / 細胞内Ca^<2+> / Ca^<2+>動員 / アセチルコリン / カルシウム / GTP結合蛋白質 |
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| Research Abstract |
It has been generally accepted that mucin release from submandibular gland is mediated by beta adrenergic receptor-adenylate cyclase system, and alpha adrenergic and muscarinic cholinergic systems are not involved in mucin release. However, we have previously shown that mucin release from dog submandibular gland is mainly mediated by muscarinic ACh receptor(mAChR)stimulation. The present study investigated signal transduction systems and GTP binding proteins coupled to mAChR for exocytosis in dog submandibular gland cells.
Mucin release was stimulated by ACh, alpha adrenergic agonists, ionomycin and thapsigardin in Ca^<2+>-dependent manner. ACh increased intracellular free Ca^<2+> concentration ( [Ca^<2+>] i), IP_3 and IP_4. IP_3, ryanodine, cyclic ADP-ribose but not caffeine stimulated Ca^<2+> release in permeabilized cells. GTPgammaS in permeabilized cells and TPA increase mucin release. GTPgammaS stimlated DTT-insensitive choline-phosphotransferase activity for platelet-activating factor (PAF) synthesis. PAF inhibited membrane Na^+, K^+-ATPase activity and mobilized Ca^<2+> in permeabilized cells.
These results suggest that mAChR stimulation causes mucin release by increasing [Ca^<2+>] i through IP_3-mediated mobilization of Ca^<2+> from intracellular stores, stimulation of Ca^<2+> induced Ca^<2+> release mechanism and activation of Ca^<2+> entry mechanism through plasma membrane. PKC and GTP binding proteins may be involved in mucin release and PAF synthesis, and serve as signal transduction systems in dog submandibular glands.
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