| Project/Area Number |
21590200
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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 |
General anatomy (including Histology/Embryology)
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| Research Institution | Iwate Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
AKUTSU Hitomi 岩手医科大学, 医学部, ポストドクター (30398482)
MATSUURA Makoto 岩手医科大学, 薬学部, 講師 (00405846)
SATOH Yoh-ichi 岩手医科大学, 医学部, 教授 (40118253)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2011: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2010: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2009: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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| Keywords | プロテアーゼ活性化型受容体 / 細胞内カルシウム変動 / 共焦点レーザー顕微鏡 / 耳下腺 / カルモジュリンキナーゼ / 細胞内カルシウムイオン / non-capacitative calcium entry / リアルタイム共焦点レーザー顕微鏡 / カルシウムイメージング / 外分泌細胞 / 外分泌機構 |
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| Research Abstract |
Protease-activated receptors(PARs) represent a novel class seven transmembrane domain G-protein coupled receptors, which are activated by proteolytic cleavage. Recent studies have reported that PARs are present in a variety of cells and have been prominently implicated in the regulation of a number of vital functions. The issue of whether the stimulation of PARs induces responses in parotid glands was examined ; with special reference to intracellular Ca^<2+>([Ca^<2+>]_i) dynamics during PARs stimulation. In the present study, PAR2 mRNA was expressed strongly in the parotid glands. In parotid acinar cells, PAR2-activating peptide(PAR2-AP), SLIGRL-NH_2, induced an increase in[Ca^<2+>]_i. Both removing of extracellular Ca^<2+> and using of Ca^<2+> channel blockers did not inhibit the PAR2-AP-induced[Ca^<2+>]_i increase. The response to PAR-2 activation was mainly caused by Ca^<2+> mobilization from intracellular Ca^<2+> stores. This peptide induced Ca^<2+> release and entry were partially inhibited by the nitric oxide synthase(NOS) inhibitor, L-NAME. The NO donor, GEA 3162, but not 8-bromo-cGMP, mimicked the effects of PAR2 in activating non capacitative calcium entry(NCCE). Both KN93(a CAM kinase II inhibitor) and W7(a calmodulin inhibitor) completely blocked a Ca^<2+> release from intracellular Ca2+store and a Ca^<2+> influx from extracellular spaces. Tetracaine and DHAB partially blocked these increases. These results indicate that PAR2-AP activates NCCE pathway. And we proposed that an effect of PAR-2 in parotid gland is dependent on CAMKII and a PAR2-AP activates the ryanodine-like receptors.
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