Atrial-specific regulation of Ca2+ channel signalosome by a lipid-binding protein
| Project/Area Number |
23790305
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General pharmacology
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| Research Institution | Toho University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2012
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | 心房 / L型Ca2+チャネル / 心房細動 / イオンチャネル / L型カルシウムチャネル / リン脂質結合タンパク質 |
|---|
| Research Abstract |
A lipid-binding protein, STARD10 is expressed and bound to L-type Ca2+ channel in the atrium but not in the ventricle. To clarify the Ca2+ channel signalosome in the atria, we analyzed the atria and their myocytes in vitro which are isolated from wild-type and STARD10 knock-out mice. The loss of STARD10 increased the current density of CaV1.2-type L-type Ca2+ currents with the enhancement of Ca2+-dependent inactivation in the atrial myocytes, but it did not change the expression of alpha1 subunit CaV1.2. The response of the isolated atria to a mechanical stretch was an increase in the contraction force in wild-type mice, while it was an increase in the rate of its spontaneous firing with suppression of development in the contraction force in knock-out mice. The results suggested that STARD10 may regulate Ca2+-dependent inactivation of atrial L-type Ca2+ current, and that the mechanism may contribute the atrial contraction force development in response to mechanical stretch.
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Report
(4 results)
Research Products
(59 results)
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[Presentation] 腎交感神経除去術の慢性房室ブロック犬の心血管系に対する作用：シルニジピンおよびアミオダロンとの比較
Author(s)
小原浩, 中村裕二, 曹新, 横山浩史, 中瀬古（泉）寛子, 安東賢太郎, 村越伸行, 佐藤明, 青沼和隆, 高原章, 池田隆徳, 杉山篤
Organizer
第８７回日本薬理学会年会
Place of Presentation
東北大学百周年記念会館川内萩ホール・仙台国際センター、宮城県仙台市
Related Report
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