| Project/Area Number |
22890049
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Legal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
UNUMA Kana 東京医科歯科大学, 大学院・医歯学総合研究科, 助教 (30586425)
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,146,000 (Direct Cost: ¥2,420,000、Indirect Cost: ¥726,000)
Fiscal Year 2011: ¥1,508,000 (Direct Cost: ¥1,160,000、Indirect Cost: ¥348,000)
Fiscal Year 2010: ¥1,638,000 (Direct Cost: ¥1,260,000、Indirect Cost: ¥378,000)
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| Keywords | 心臓性突然死 / コネキシン / ギャップジャンクション / 情動ストレス / connexin43 / α-アドレナリン受容体 / 細胞間情報伝達 / ストレス / アドレナリン受容体 / miRNA |
|---|
| Research Abstract |
Immobilization(IMO) confers emotional stress in animals and humans. It was recently reported that IMO in rats induced translocation of connexin-43(Cx43) to gap junctions(GJs) and attenuated arrhythmogenesis with GJ inhibition. Few reports show the contribution of adrenoceptors to Cx43 upregulation in cardiomyocytes, but the involvement of adrenoceptors and ischemia in Cx43 translocation in IMO remains elusive. Male Sprague-Dawley rats underwent IMO and the ventricular distribution of Cx43 was examined by western blotting. IMO induced translocation of Cx43 to the GJ-enriched membrane fraction, with a peak at 60min. The IMO-induced Cx43 translocation was inhibited by pretreatment with theα-adrenoceptor. Theβ-blockers inhibited the premature ventricular contractions(PVCs) induced by IMO. Translocation of Cx43 to the GJ-enriched fraction occurs via theα-adrenoceptor pathway, independently of ischemia. Theβ-adrenoceptor pathway contributes to the inducing of PVCs in IMO
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