2014 Fiscal Year Final Research Report
TRIC channels and calcium release from endo/sarcoplasmic reticulum
Project/Area Number |
24680041
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Research Category |
Grant-in-Aid for Young Scientists (A)
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Allocation Type | Partial Multi-year Fund |
Research Field |
Neurophysiology and muscle physiology
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Research Institution | Kyoto University |
Principal Investigator |
YAMAZAKI Daiju 京都大学, 生理化学研究ユニット, 特定講師 (40467428)
|
Project Period (FY) |
2012-04-01 – 2015-03-31
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Keywords | TRICチャネル / 小胞体 / カウンターイオン / 平滑筋 / カルシウムスパーク / 過分極シグナル |
Outline of Final Research Achievements |
In this study, it was revealed the following three points using smooth muscle cells having both TRIC channel subtypes and Ca2+ release channels including ryanodine cereptor (RyR) and inositol-1,4,5-trisphosphate receptor (IP3R). 1) Overexpression of TRIC-A enhanced hyperpolarization signaling which evoked by Ca2+ spark, and showed hypotension induced by constitutively vascular relaxation. 2) It was suggested that TRIC-A expression level in vascular smooth muscle cells controlled blood pressure. 3) It was suggested that TRIC-A expression level in vascular smooth muscle cells also affected the amount of Ca2+ contents in the endo/sarcoplasmic reticulum which distributed RyR and/or IP3R.
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Free Research Field |
生理学・薬理学
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