Information control for a linkage between macro cardiac function and gene expression: physiomic analysis of responses to oxygen environment

2016 Fiscal Year Final Research Report

• Project/Area Number: 26282127
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: Biomedical engineering/Biomaterial science and engineering
• Research Institution: Kawasaki Medical School
• Principal Investigator: Mohri Satoshi 川崎医科大学, 医学部, 教授 (00294413)
• Co-Investigator(Kenkyū-buntansha): 片野坂 友紀 岡山大学, 医歯(薬)学総合研究科, 助教 (60432639) ; 橋本 謙 川崎医科大学, 医学部, 講師 (80341080) ; 氏原 嘉洋 川崎医科大学, 医学部, 助教 (80610021)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 細胞分裂 / 胎児酸素環境 / 心筋細胞 / 胎児循環 / 分裂促進因子 / 心筋肥大 / 後期促進複合体

Outline of Final Research Achievements

It is important to investigate the mechanisms of cell division and the regulation of energy consumption of cardiomyocyte for cardiovascular medicine. We identified Fam64a as an novel essential molecule for caudiomyocyte division. Fam64a was abundantly expressed in hypoxic fetal cardiomyocyte nuclei, but was sharply repressed by oxygen exposure, and also in postnatal cardiomyocytes. Fam64a knockdown inhibited and its overexpression enhanced the proliferation of cardiomyocytes. Non-degradable Fam64a mutant suggested that its optimum expression and subsequent degradation by anaphase-promoting complex/cyclosome before anaphase are required for cell division. Moreover, we revealed that short term triiodothyronine(T3) administration increased SERCA2 expression and decreased NCX1 expression but did not change cardiac contractility, resulting in energy-saving oxygen consumption for excitation-contraction coupling. Long term T3 administration decreased cardiac contractility and NCX activity.

Free Research Field

生体医工学