Research Papers:

NOGO-B promotes EMT in lung fibrosis via MMP14 mediates free TGF-beta1 formation

Ye Xiong, Jing Zhang, Lingzhi Shi, Yunye Ning, Ying Zhu, Si Chen, Meng Yang, Jingyu Chen, Guo-Wu Zhou _ and Qiang Li

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Oncotarget. 2017; 8:71024-71037. https://doi.org/10.18632/oncotarget.20297

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Ye Xiong1,*, Jing Zhang2,*, Lingzhi Shi3,4,*, Yunye Ning1, Ying Zhu1, Si Chen1, Meng Yang1, Jingyu Chen4, Guo-Wu Zhou1,6 and Qiang Li1,5

1Department of Respiratory Medicine, Changhai Hospital, Second Military Medical University, Shanghai, China

2Department of Pathology, Changhai Hospital, Second Military Medical University, Shanghai, China

3Department of Respiratory Medicine, Wuxi People Hospital, Nanjing Medical University, Nanjing, China

4Jiangsu Province Key Laboratory of Organ Transplantation, Wuxi People Hospital, Nanjing Medical University, Nanjing, China

5Department of Respiratory Medicine, Shanghai First Hospital, Shanghai Jiaotong University, Shanghai, China

6National Clinical Research Center for Respiratory Diseases, Center for Respiratory Diseases, Department of Pulmonary and Critical Care Medicine, China-Japan Friendship Hospital, Beijing, China

*Authors contributed equally to this work

Correspondence to:

Guo-Wu Zhou, email: [email protected]

Qiang Li, email: [email protected]

Keywords: Nogo-b, MMP14, idiopathic pulmonary fibrosis (IPF), epithelial mesenchymal transition (EMT), TGF-beta1

Abbreviations: Nogo-b: reticulon 4-b; MMP14: matrix metallopeptidase 14; IPF: Idiopathic pulmonary fibrosis; EMT: Epithelial mesenchymal transition; TGFbeta1: transforming growth factorbeta 1

Received: April 04, 2017     Accepted: July 19, 2017     Published: August 16, 2017


Idiopathic pulmonary fibrosis (IPF) is a lung disease with an extremely poor prognosis. Epithelial mesenchymal transition (EMT) appearing on the airway epithelial cell plays an essential role in the formation and development of Idiopathic pulmonary fibrosis. In this paper, Bleomycin (BLM)-induced mice model combined with bioinformatics analysis were employed to elucidate the potential mechanism of EMT in pulmonary fibrosis. The obtained results showed that endoplasmic reticulum protein Nogo-b may promote MMP14-mediated proprotein maturation of TGF-β1, accelerating the release of free TGF-β1 in type II airway epithelial cells A549, subsquently, induce the epithelial-mesenchymal transition (EMT) of the cell. In all, the overexpression of Nogo-b play a role in the course of pulmonary fibrosis by influencing the EMT ability of cells.

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