Investigation on possible link between Ist and CaV1.3 RNA editing
| Project/Area Number |
23590258
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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 |
General physiology
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| Research Institution | Shiga University of Medical Science |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
MATSUURA Hiroshi 滋賀医科大学, 医学部, 教授 (60238962)
DING Wei-guang 滋賀医科大学, 医学部, 助教 (80242973)
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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 |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
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| Keywords | 心臓 / ペースメーカー / 洞房結節 / イオンチャネル / 洞房結節細胞 / ペースメーカー機序 / 膜電流 / 国際情報交換（フランス） / 心臓ペースメーカー |
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| Research Abstract |
The sustained inward Na+ current (Ist) in sinoatrial node (SAN) pacemaker cells has been suggested to contribute to the pacemaker activity, although unknown molecular correlates of this current limits the understanding of its significance in the pacemaker activity. The purpose of this study was 1) to examine the relationship between L-type Ca2+ channel CaV1.3 subunit and Ist in their functional expression levels, and 2) to identify the RNA editing-mediated CaV1.3 variants. The density of Ist was positively correlated with the magnitude of L-type Ca2+ current (ICa,L). In knock-out mice with disruption of CaV1.3, ICa,L was significantly reduced, which was accompanied by a complete loss of Ist. Comprehensive analysis of CaV1.3 transcripts using the second generation sequencer revealed the presence of rare variants with residue changes in the Ca2+ selectivity filter. These findings suggest that Ist is mediated by CaV1.3 variants Ist in SAN pacemaker cells.
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Report
(4 results)
Research Products
(14 results)
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[Journal Article] A novel KCNQ1 missense mutation identified in a patient with juvenile-onset atrial fibrillation causes constitutively open IKs channels.2014
Author(s)
Hasegawa K, Ohno S, Ashihara T, Itoh H, Ding WG, Toyoda F, Makiyama T, Aoki H, Nakamura Y, Delisle BP, Matsuura H, Horie M.
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Journal Title
Heart Rhythm
Volume: 11
Issue: 1
Pages: 67-75
DOI
Related Report
Peer Reviewed
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[Journal Article] The G-protein-gated K+ channel, IKACh, is required for regulation of pacemaker activity and recovery of resting heart rate after sympathetic stimulation.2013
Author(s)
Mesirca P, Marger L, Toyoda F, Rizzetto R, Audoubert M, Dubel S, Torrente AG, Difrancesco ML, Muller JC, Leoni AL, Couette B, Nargeot J, Clapham DE, Wickman K, Mangoni ME.
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Journal Title
Journal of General Physiology
Volume: 142
Issue: 2
Pages: 113-126
DOI
Related Report
Peer Reviewed
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