| Project/Area Number |
23592585
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Ophthalmology
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| Research Institution | Iwate Medical University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
SAINO Tomoyuki 岩手医科大学, 医学部, 教授 (40305991)
SATOH Yoh-ichi 岩手医科大学, 医学部, 教授 (40118253)
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| Co-Investigator(Renkei-kenkyūsha) |
KUROSAKA Daijiro 岩手医科大学, 医学部, 教授 (20215099)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 涙腺 / プロテアーゼ活性化型受容体 / 細胞内カルシウムイオン / 共焦点レーザー顕微鏡 / RT-PCR / 外分泌 / calcium entry / カルシウムシグナリング / 涙液分泌機構 / カルシウム流入機構 |
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| Research Abstract |
Protease-activated receptors (PARs) are G-protein-coupled receptors, activated by proteolytic cleavage. Here, lacrimal gland acinar cell responses to PAR activation were examined, with respect to intracellular Ca2+ concentration ([Ca2+]i) dynamics. Only PAR2 mRNA was detected in these acinar cells. A PAR2-activating peptide (PAR2-AP) induced an increase in [Ca2+]i in these cells. The removal of extracellular Ca2+ and the use of Ca2+ channel blockers did not inhibit PAR2-AP-induced [Ca2+]i increases. The NO donor mimicked the effects of PAR2 in activating non-capacitative calcium entry (NCCE). However, both calyculin A and a low concentration of Gd3+ did not completely block the PAR2-AP-induced increase in [Ca2+]i. These findings indicated that PAR2 activation resulted primarily in Ca2+ mobilization from intracellular Ca2+ stores and that PAR2-mediated [Ca2+]i changes were mainly independent of IP3. We suggest that PAR2-AP differentially regulates both NCCE and CCE, predominantly NCCE.
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