Degenerative therapy for heart failure using skeletal muscle cell-extracellular matrix interaction.

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08401
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Experimental pathology
• Research Institution: Osaka University
• Principal Investigator: Kawaguchi Naomasa 大阪大学, 医学系研究科, 特任准教授(常勤) (70224748)
• Co-Investigator(Kenkyū-buntansha): 濱田 吉之輔 大阪大学, 医学系研究科, 特任准教授 (10362683) ; 内仲 彩子 名古屋大学, 医学系研究科(保健), 助教 (40746921) ; 松浦 成昭 大阪大学, 医学系研究科, 教授 (70190402) ; 森 誠司 大阪大学, 医学系研究科, 招へい教授 (90467506)
• Co-Investigator(Renkei-kenkyūsha): MIYAGAWA Shigeru 大阪大学, 医学系研究科, 特任教授 (70544237)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 再生医学

Outline of Final Research Achievements

Skeletal myoblast sheet transplantation, a method used for treating failing hearts, results in the secretion of cytokines that improve heart function. Enhancing the survival rate of implanted myoblasts should lead to more continuous and effective therapies. We hypothesized that laminin 211, which binds to α-dystroglycan on muscle cells, could inhibit dropout of implanted myoblasts from host myocardia. Laminin 211 expressed-fibroblasts and skeletal myoblasts multi-layered sheet were transplanted for an ischemic cardiomyopathy model rat. Laminin 211 secreted by implanted fibroblasts inhibited the dropout of implanted myoblasts from grafted myocardia, resulting in more permanent therapeutic effects upon myoblast sheet transplantation. This approach using laminin 211 could have been expected the application for the cell-based transplantation such as cardiomyocyte derived from induced pluripotent stem cells.

Free Research Field

心臓血管病理学