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Treatment of acute lung injury by targeting MG53-mediated cell membrane repair

Author

Listed:
  • Yanlin Jia

    (Merck Research Lab)

  • Ken Chen

    (Daping Hospital, The Third Military Medical University, Chongqing Institute of Cardiology)

  • Peihui Lin

    (Davis Heart and Lung Research Institute, The Ohio State University
    Robert Wood Johnson Medical School)

  • Gissela Lieber

    (Merck Research Lab)

  • Miyuki Nishi

    (Kyoto University Graduate School of Pharmaceutical Sciences)

  • Rosalie Yan

    (TRIM-edicine, Inc.)

  • Zhen Wang

    (Daping Hospital, The Third Military Medical University, Chongqing Institute of Cardiology)

  • Yonggang Yao

    (Daping Hospital, The Third Military Medical University, Chongqing Institute of Cardiology)

  • Yu Li

    (Daping Hospital, The Third Military Medical University, Chongqing Institute of Cardiology)

  • Bryan A. Whitson

    (Davis Heart and Lung Research Institute, The Ohio State University)

  • Pu Duann

    (Davis Heart and Lung Research Institute, The Ohio State University)

  • Haichang Li

    (Davis Heart and Lung Research Institute, The Ohio State University)

  • Xinyu Zhou

    (Davis Heart and Lung Research Institute, The Ohio State University)

  • Hua Zhu

    (Davis Heart and Lung Research Institute, The Ohio State University
    Robert Wood Johnson Medical School)

  • Hiroshi Takeshima

    (Kyoto University Graduate School of Pharmaceutical Sciences)

  • John C. Hunter

    (Merck Research Lab)

  • Robbie L. McLeod

    (Merck Research Lab)

  • Noah Weisleder

    (Robert Wood Johnson Medical School
    TRIM-edicine, Inc.
    Davis Heart and Lung Research Institute, The Ohio State University)

  • Chunyu Zeng

    (Daping Hospital, The Third Military Medical University, Chongqing Institute of Cardiology)

  • Jianjie Ma

    (Davis Heart and Lung Research Institute, The Ohio State University
    Robert Wood Johnson Medical School
    TRIM-edicine, Inc.)

Abstract

Injury to lung epithelial cells has a role in multiple lung diseases. We previously identified mitsugumin 53 (MG53) as a component of the cell membrane repair machinery in striated muscle cells. Here we show that MG53 also has a physiological role in the lung and may be used as a treatment in animal models of acute lung injury. Mice lacking MG53 show increased susceptibility to ischaemia–reperfusion and overventilation-induced injury to the lung when compared with wild-type mice. Extracellular application of recombinant human MG53 (rhMG53) protein protects cultured lung epithelial cells against anoxia/reoxygenation-induced injuries. Intravenous delivery or inhalation of rhMG53 reduces symptoms in rodent models of acute lung injury and emphysema. Repetitive administration of rhMG53 improves pulmonary structure associated with chronic lung injury in mice. Our data indicate a physiological function for MG53 in the lung and suggest that targeting membrane repair may be an effective means for treatment or prevention of lung diseases.

Suggested Citation

  • Yanlin Jia & Ken Chen & Peihui Lin & Gissela Lieber & Miyuki Nishi & Rosalie Yan & Zhen Wang & Yonggang Yao & Yu Li & Bryan A. Whitson & Pu Duann & Haichang Li & Xinyu Zhou & Hua Zhu & Hiroshi Takeshi, 2014. "Treatment of acute lung injury by targeting MG53-mediated cell membrane repair," Nature Communications, Nature, vol. 5(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms5387
    DOI: 10.1038/ncomms5387
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    Cited by:

    1. Yuemin Ma & Lei Ding & Zhenhai Li & Chun Zhou, 2023. "Structural basis for TRIM72 oligomerization during membrane damage repair," Nature Communications, Nature, vol. 14(1), pages 1-13, December.

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