2010 Fiscal Year Final Research Report
Research on the molecular mechanism underlying sudden cardiac deaths due to toxic substanses, ischemia and emotional stress
| Project/Area Number |
20390193
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Legal medicine
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| Research Institution | The University of Tokyo |
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Principal Investigator |
YOSHIDA Ken-ichi The University of Tokyo, 大学院・医学系研究科, 教授 (40166947)
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| Co-Investigator(Kenkyū-buntansha) |
UEYAMA Takashi 和歌山県立医科大学, 医学部, 准教授 (50264875)
KIMURA Hiroko 順天堂大学, 医学部, 准教授 (00053299)
UEMURA Kouichi 東京医科歯科大学, 医歯学総合研究科, 教授 (30244586)
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| Co-Investigator(Renkei-kenkyūsha) |
HARADA Kazuki 東京大学, 大学院・医学系研究科, 講師 (00253146)
SHINTANI Kaori 東京大学, 大学院・医学系研究科, 助教 (50345047)
SAKA Kanju 東京大学, 大学院・医学系研究科, 技術職員 (30447388)
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| Project Period (FY) |
2008 – 2010
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| Keywords | コネクシン43 / ギャップ結合 / 不整脈 / 心臓突然死 / 心筋虚血 / 心理ストレス / 身体拘束 / 心筋梗塞 |
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| Research Abstract |
In rats, we found that ischemia induces Connexin-43 (Cx43) translocation to gap junction (GJ) and Phospholamaban (PLB) dephosphorylation, and reperfusion promotes spreading of Contraction Bands (CBs). We also found that anti-PLB antibody injection enlarges myocardial infarction through mPTP opening. In restrain of rats, Cx43 was translocated to the GJs, thereby reducing premature ventricular contractions and promoting GJ communication. As a result, lethal arrhythmias were suppressed.
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