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2015 Fiscal Year Final Research Report

Effects of fetal gene reprogramming on expression, distribution and expression of gap junction in failing hearts

Research Project

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Project/Area Number 26860215
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Pathological medical chemistry
Research InstitutionOita University

Principal Investigator

Takanari Hiroki  大分大学, 医学部, 助教 (70723253)

Research Collaborator Marcel van der Heyden  University Medical Center Utrecht, Department of Medical Physiology, Division of heart and Lungs, Associate Professor
Toon van Veen  University Medical Center Utrecht, Department of Medical Physiology, Division of heart and Lungs, Associate Professor
Vos Marc  University Medical Center Utrecht, Department of Medical Physiology, Division of heart and Lungs, Professor
Project Period (FY) 2014-04-01 – 2016-03-31
Keywords心筋ギャップ結合 / Connexin43 / Connexin40 / カルモデュリン / CaMK-II / 脂質負荷
Outline of Final Research Achievements

Gap junction in the heart tissue contributes to the intercellular communication between adjucent cardiomyocytes. Gap junction channel consists of connexin43 protein (Cx43) in ventricle. We examined the molecular mechanisms which control the expression and the subcellular distribution of Cx43 in the heart. Unfortunately, we could not find any apparent molecules from fetal gene program which could influence the expression of Cx43 expression. Calcium handling protein and protein kinase depends to it modified the distribution of Cx43 in the heart, which resulted in alteration of electrical conductance of the heart tissue. Cholesterol did not affect the expression of Cx43, while mRNA level of connexin40 protein was significantly decreased by cholesterol application. The result suggested the relation between lipid metabolism disorder and cardiac arrhythmias such as atrial fibrillation.

Free Research Field

心臓電気生理学

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Published: 2017-05-10  

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