The molecular and cellular mechanism of myocardial repair/regeneration

2016 Fiscal Year Final Research Report

• Project/Area Number: 26293054
• Research Category: Grant-in-Aid for Scientific Research (B)
• Allocation Type: Partial Multi-year Fund
• Section: 一般
• Research Field: General pharmacology
• Research Institution: Osaka University
• Principal Investigator: FUJIO Yasushi 大阪大学, 薬学研究科(研究院), 教授 (20359839)
• Co-Investigator(Kenkyū-buntansha): 毛利 友美 大阪大学, 薬学研究科(研究院), 研究員 (20572960) ; 中山 博之 大阪大学, 薬学研究科(研究院), 准教授 (40581062)
• Project Period (FY): 2014-04-01 – 2017-03-31
• Keywords: 心臓 / 組織修復・再生 / 心筋細胞増殖 / 細胞骨格

Outline of Final Research Achievements

As mammalian cardiomyocytes substantially cease to proliferate immediately after birth, it has been believed that adult mammalian hearts show only limited regenerative capacities. However, clinically, most cases of acute myocarditis are self-limiting with myocardial recovery. Thus, we hypothesized that adult cardiomyocytes might restore regenerative activities during the healing process of myocarditis. In this study, using experimental autoimmune myocarditis (EAM) model, we addressed this hypothesis from two viewpoints; One is phenotypic modulation of cardiomyocytes and the other is cardiomyocyte proliferation. As for phenotypic modulation, proteomics analysis revealed that the expression of moesin, a cytoskeletal protein, was upregulated in cardiomyocytes, leading to the protrusion formation. As for cell proliferation, we detected cell cycle marker-positive cardiomyocytes at the beginning of the myocardial recovery, proposing the unexpected adult cardiomyocyte proliferation.

Free Research Field

循環薬理学