Abstract
Deficiency of TOM5, a mitochondrial protein, causes organizing pneumonia (OP) in mice. The clinical significance and mechanisms of TOM5 in the pathogenesis of OP remain elusive. We demonstrated that TOM5 was significantly increased in the lung tissues of OP patients, which was positively correlated with the collagen deposition. In a bleomycin-induced murine model of chronic OP, increased TOM5 was in line with lung fibrosis. In vitro, TOM5 regulated the mitochondrial membrane potential in alveolar epithelial cells. TOM5 reduced the proportion of early apoptotic cells and promoted cell proliferation. Our study shed light on the roles of TOM5 in OP.
Keywords:
Organizing pneumonia; TOM5; alveolar epithelial cells; mitochondrial membrane potential; bleomycin.
MeSH terms
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Alveolar Epithelial Cells* / metabolism
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Alveolar Epithelial Cells* / pathology
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Animals
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Apoptosis
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Cell Proliferation
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Cryptogenic Organizing Pneumonia / metabolism
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Cryptogenic Organizing Pneumonia / pathology
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Disease Models, Animal
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Female
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Humans
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Male
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Membrane Potential, Mitochondrial* / physiology
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Mice
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Mice, Inbred C57BL
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Mitochondrial Precursor Protein Import Complex Proteins
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Organizing Pneumonia
Substances
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Mitochondrial Precursor Protein Import Complex Proteins
Grants and funding
Research reported in this publication was supported by the Precision Medicine Research of the National Key Research and Development Plan of China (2016YFC0905800), the National Natural Science Foundation of China (81770031, 81970031, 82171738), the Natural Science Foundation of Jiangsu Province (BK20171501, BK2017080, and BK20181497), Jiangsu Province’s Young Medical Talent Program, China (QNRC2016600), the Jiangsu Provincial Health and Family Planning Commission Foundation (Q2017001), and the Science and technology project of Changzhou Health and Construction Commission (QN202360).