| Project/Area Number |
17590954
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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 |
Endocrinology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TAKANO Koji The University of Tokyo, Faculty of Medicine, Assistant Professor, 医学部附属病院, 助手 (20236243)
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| Project Period (FY) |
2005 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2005: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Ion channels / Endocrine cells / Hormone secretion / Pituitary cells / growth hormone / ghrelin / IGF-1 / 下垂体細胞 / 下垂体前葉細胞 / 電気生理 / チャネル / 陽イオンチャネル / 副腎皮質細胞 / adrenomedullin / ACTH |
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| Research Abstract |
The significance of nonselective cation current in hormone secretion from anterior pituitary cells was investigated. Fusion gene of GH and yellow fluorescent protein was transfected into GH3 cells. Fusion protein was expressed in exocytotic vesicles and was observed by confocal microscope. Exocytotic events were visualized by confocal imaging of the fluorescent fusion protein. Depolarization by high extracellular K stimulated exocytosis. Nitrendipine, a blocker of L-type voltage-gated calcium channel almost abolished high K-induced exocytosis. TRH also stimulated the exocytosis that was attenuated by nitrendipine. Replacing the extracellular sodium by inert cation tetramethylammonium attenuated the TRH-induced exocytosis suggesting the role of nonselective cation current on the exocytotic events.
After the exocytotic events, hormone in the exocytotic vesicles should be refilled by activating the de-novo transcription of hormone. The transcription activation of GH was inventigated in GH3 by luciferase assay. Stimulators of exocytosis also stimulated transctiption activation in these cells. Regulators of hormone secretion such as calcium influx through L-type voltage-gated calcium channels and PKA were also involved in the regulation of GH transcription regulation.
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