TOM5 regulates the mitochondrial membrane potential of alveolar epithelial cells in organizing pneumonia
Yan Qian,
Xiao Li,
Xinyu Li,
Xijie Zhang,
Qi Yuan,
Zhengxia Wang,
Mingshun Zhang,
Mao Huang,
Ningfei Ji
Affiliations
Yan Qian
Department of Respiratory and Critical Care Medicine, The Affiliated Changzhou No. 2 People's Hospital of Nanjing Medical University, Changzhou, People’s Republic of China
Xiao Li
Department of Pathology, Jiangsu Province Hospital and Nanjing Medical University First Affiliated Hospital, Nanjing, People’s Republic of China
Xinyu Li
NHC Key Laboratory of Antibody Technique, Department of Immunology, Nanjing Medical University, Nanjing, People’s Republic of China
Xijie Zhang
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China
Qi Yuan
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China
Zhengxia Wang
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China
Mingshun Zhang
NHC Key Laboratory of Antibody Technique, Department of Immunology, Nanjing Medical University, Nanjing, People’s Republic of China
Mao Huang
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China
Ningfei Ji
Department of Respiratory and Critical Care Medicine, The First Affiliated Hospital of Nanjing Medical University, Nanjing, People’s Republic of China
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.
