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

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 Takeshima, John C. Hunter, Robbie L. McLeod, Noah Weisleder, Chunyu Zeng () and Jianjie Ma ()
Additional contact information
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
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
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
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

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: 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.

Date: 2014
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DOI: 10.1038/ncomms5387

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