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

Research Project

Project/Area Number 15K08401
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Experimental pathology
Research InstitutionOsaka 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
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2017: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2016: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords再生医学 / 再生医療
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.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report
  • Research Products

    (2 results)

All 2015

All Journal Article (2 results) (of which Peer Reviewed: 2 results,  Open Access: 1 results)

  • [Journal Article] SVVYGLR motif of the thrombin-cleaved N-terminal osteopontin fragment enhances the synthesis of collagen type III in myocardial fibrosis.2015

    • Author(s)
      Uchinaka A, Hamada Y, Mori S, Miyagawa S, Saito A, Sawa Y, Matsuura N, Yamamoto H, Kawaguchi N
    • Journal Title

      Mol Cell Biochem

      Volume: 408 Issue: 1-2 Pages: 191-203

    • DOI

      10.1007/s11010-015-2495-y

    • Related Report
      2015 Research-status Report
    • Peer Reviewed
  • [Journal Article] Improvement of cardiac function after implanting the osteopontin-derived peptide SVVYGLR in a hamster model of dilated cardiomyopathy.2015

    • Author(s)
      Mizuno Y, Uchinaka A, Horii Y, Mori S, Hamada Y, Miyagawa S, Saito A, Sawa Y, Matsuura N, Kawaguchi N
    • Journal Title

      Interact Cardiovasc Thorac Surg

      Volume: 21 Issue: 4 Pages: 506-514

    • DOI

      10.1093/icvts/ivv197

    • Related Report
      2015 Research-status Report
    • Peer Reviewed / Open Access

URL: 

Published: 2015-04-16   Modified: 2019-03-29  

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