Development of a novel method for the regeneration of the cavernous body by regulating micro RNA expression

2018 Fiscal Year Final Research Report

• Project/Area Number: 15K10618
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Urology
• Research Institution: The University of Tokyo
• Principal Investigator: Nishimatsu Hiroaki 東京大学, 医学部附属病院, 登録診療員 (60251295)
• Co-Investigator(Kenkyū-buntansha): 鈴木 越 聖マリアンナ医科大学, 医学研究科, 講師 (40313134)
• Project Period (FY): 2015-04-01 – 2019-03-31
• Keywords: 動脈硬化 / プラーク内出血 / 炎症性サイトカイン

Outline of Final Research Achievements

The rupture of plaques in atherosclerotic lesion causes the obstruction of the coronary artery, leading to acute myocardial infarction. Therefore, it is pivotal to establish a method to prevent plaque rupture. It is well known that plaques with thin-cap fibroatheroma is vulnerable to damages and often rupture. Intraplaque hemorrhage (IPH) is regarded as a major factor that triggers the instability and vulnerability of plaques. We found that the proinflammatory cytokine interleukin-1beta（IL-1beta）is implicated in IPH using a mouse model of atherosclerosis. We also found that IL-1beta inhibits normal angiogenesis and stimulates immature angiogenesis, which results in the leakage of erythrocytes from new vessels in the plaques and IPH.

Free Research Field

泌尿器科学、勃起不全

Academic Significance and Societal Importance of the Research Achievements

急性心筋梗塞は代表的な心血管病であり発症を防ぐことは国民の健康寿命を延ばすために重要である。今回我々はマウスのモデルではあるが炎症性サイトカインであるinterleukin-1beta（IL-1beta）の発現を抑制すると急性心筋梗塞の発症を予防できる可能性を示すことができた。今後IL-1betaの阻害薬あるいは活性阻害抗体薬などが開発されることを期待したい。