TRIC channels and calcium release from endo/sarcoplasmic reticulum

2014 Fiscal Year Final Research Report

• Project/Area Number: 24680041
• Research Category: Grant-in-Aid for Young Scientists (A)
• Allocation Type: Partial Multi-year Fund
• Research Field: Neurophysiology and muscle physiology
• 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
• 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.

Free Research Field

生理学・薬理学