Study on the drug exercise therapy that is effective for cardiac hypertrophy heart failure that develops in Ca2 + load model mouse

2016 Fiscal Year Final Research Report

• Project/Area Number: 15K18975
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: General physiology
• Research Institution: National Cardiovascular Center Research Institute
• Principal Investigator: JIN MEIHUA 国立研究開発法人国立循環器病研究センター, 研究所, 研究員 (40746773)
• Co-Investigator(Renkei-kenkyūsha): Wakabayashi Shigeo 大阪医科大学, 医学研究科・薬理学教室, 研究員 (70158583)
• Research Collaborator: Shirai Mikiyasu 国立循環器病研究センター, 肺高血圧症先端医学研究部, 特任研究員 (70162758)
• Project Period (FY): 2015-04-01 – 2017-03-31
• Keywords: heart failure / hypertrophy / hypoxia / Ca2+-binding protein

Outline of Final Research Achievements

Since Na+ / H+ exchanger (NHE1)-overexpressed mice are difficult to reproduce, we modified the original schedule. Using knockout mice, we analyzed the function of calcineurin B-like protein (CHP) 3 which were closely related to NHE1 in vivo. The results indicated that the cardiac function and the cardiac weight of CHP3-deficient mice at the baseline were not different from those of the wild type mice. A chronic hypoxia induced the right ventricle hypertrophy in the wild-type mice. In contrast, interestingly, in addition to the right ventricle it caused a significant left ventricle hypertrophy in the CHP3-deficient mice. In addition, since the expression of CHP3 in the heart of the wild type mice was markedly decreased by hypoxia. Thus, it was suggested that CHP3 could be an important molecule that might negatively regulate cardiac hypertrophy caused by hypoxic stimulation, by controlling the expression level.

Free Research Field

循環器