2015 Fiscal Year Final Research Report
Molecular mechanism of Takotsubo cardiomyopathy
| Project/Area Number |
24249048
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| Research Category |
Grant-in-Aid for Scientific Research (A)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Circulatory organs internal medicine
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| Research Institution | Keio University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
ARAI TAKAHIDE 慶應義塾大学, 医学部, 助教 (00383894)
KANAZAWA HIDEAKI 慶應義塾大学, 医学部, 特任講師 (40338033)
SUKEGAWA HIROAKI 慶應義塾大学, 医学部, 助教 (60535607)
TABEI RYOTA 慶應義塾大学, 医学部, 助教 (20573322)
MUNAKATA MASAHITO 慶應義塾大学, 医学部, 共同研究員 (40445284)
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| Project Period (FY) |
2012-04-01 – 2016-03-31
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| Keywords | 脳心連関 |
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| Outline of Final Research Achievements |
Big emotional or physical stress may lead to an imbalance in the brain, resulting in Takotsubo cardiomyopathy (TC), transient left ventricular (LV) apical ballooning. We first confirmed the central neurons of cardiac sympathetic nerves in the hypothalamus innervating the LV apex, and investigated the changes in gene expression in an animal model of TC induced by epilepsy, a clinical trigger of TC. We found that chemokine ligand 2 (Ccl2) strongly stimulated the central neurons of the cardiac sympathetic nerves. Consequent upstream sympathetic activation induced significant upregulation of neuropeptide Y (NPY) in the left stellate ganglion (LSG) and cardiac sympathetic nerves. Administration of Ccl2 into the central neurons evoked TC and increased NPY at LSG. Overall, our results provide the first evidence as to how emotional or physical stress translates into molecular signals in the brain, leading to LV apical ballooning.
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| Free Research Field |
分子生物学
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