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MicroRNA29a regulates IL-33-mediated tissue remodelling in tendon disease

Author

Listed:
  • Neal L. Millar

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow)

  • Derek S. Gilchrist

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow)

  • Moeed Akbar

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow)

  • James H. Reilly

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow)

  • Shauna C. Kerr

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow)

  • Abigail L. Campbell

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow)

  • George A. C. Murrell

    (Orthopaedic Research Institute, St George Hospital Campus, University of New South Wales)

  • Foo Y. Liew

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow
    School of Biology and Basic Medical Sciences, Soochow University)

  • Mariola Kurowska-Stolarska

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow)

  • Iain B. McInnes

    (Institute of Infection, Immunity and Inflammation, College of Medicine, Veterinary and Life Sciences University of Glasgow)

Abstract

MicroRNA (miRNA) has the potential for cross-regulation and functional integration of discrete biological processes during complex physiological events. Utilizing the common human condition tendinopathy as a model system to explore the cross-regulation of immediate inflammation and matrix synthesis by miRNA we observed that elevated IL-33 expression is a characteristic of early tendinopathy. Using in vitro tenocyte cultures and in vivo models of tendon damage, we demonstrate that such IL-33 expression plays a pivotal role in the transition from type 1 to type 3 collagen (Col3) synthesis and thus early tendon remodelling. Both IL-33 effector function, via its decoy receptor sST2, and Col3 synthesis are regulated by miRNA29a. Downregulation of miRNA29a in human tenocytes is sufficient to induce an increase in Col3 expression. These data provide a molecular mechanism of miRNA-mediated integration of the early pathophysiologic events that facilitate tissue remodelling in human tendon after injury.

Suggested Citation

  • Neal L. Millar & Derek S. Gilchrist & Moeed Akbar & James H. Reilly & Shauna C. Kerr & Abigail L. Campbell & George A. C. Murrell & Foo Y. Liew & Mariola Kurowska-Stolarska & Iain B. McInnes, 2015. "MicroRNA29a regulates IL-33-mediated tissue remodelling in tendon disease," Nature Communications, Nature, vol. 6(1), pages 1-13, November.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7774
    DOI: 10.1038/ncomms7774
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