Effects of IL-18 on pressure overloaded-heart
Project/Area Number |
26461136
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Cardiovascular medicine
|
Research Institution | Hyogo Medical University |
Principal Investigator |
|
Co-Investigator(Kenkyū-buntansha) |
岩破 俊博 兵庫医科大学, 医学部, 助教 (00648230)
西村 晃一 兵庫医科大学, 医学部, 病院助手 (30724116)
|
Project Period (FY) |
2014-04-01 – 2017-03-31
|
Project Status |
Completed (Fiscal Year 2016)
|
Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
|
Keywords | IL-18 / pressure overload / energy homeostasis / インターロイキン18 / 圧負荷 / エネルギー代謝 / 心不全 / 脂肪酸代謝 / LPL / 分子心臓病学 / 圧負荷ストレス |
Outline of Final Research Achievements |
Effects of IL-18 on pressure overloaded-heart have yet to be revealed. We introduced pressure overload by transverse aortic constriction (TAC) to wild type mice and IL-18 knockout mice. IL-18 knockout mice exhibited higher mortality and severer left ventricular remodeling after TAC. We examined myocardial AMPK activity. While TAC elevated AMPK activity in wild type heart, it did not in Il-18 heart. Therefore, we administered AMPK direct activator, AICAR, to IL-18 knockout mice. The administration attenuated higher mortality and severer left ventricular remodeling after TAC compared with wild type mice. These data suggest that IL-18 maturation by TAC activates AMPK and fatty acid metabolism, leading to adaptation to acute pressure overload.
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Report
(4 results)
Research Products
(4 results)