Nix/BNIP3L‐dependent mitophagy accounts for airway epithelial cell injury induced by cigarette smoke
2019
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- Autor(en) / Beteiligte
- Titel
- Nix/BNIP3L‐dependent mitophagy accounts for airway epithelial cell injury induced by cigarette smoke
- Ist Teil von
- Journal of cellular physiology, 2019-08, Vol.234 (8), p.14210-14220
- Ort / Verlag
- United States: Wiley Subscription Services, Inc
- Erscheinungsjahr
- 2019
- Quelle
- Wiley Online Library Journals Frontfile Complete
- Beschreibungen/Notizen
- Cigarette smoke‐induced airway epithelial cell mitophagy is an important mechanism in the pathogenesis of chronic obstructive pulmonary disease (COPD). Mitochondrial protein Nix (also known as BNIP3L) is a selective autophagy receptor and participates in several human diseases. However, little is known about the role of Nix in airway epithelial cell injury during the development of COPD. The aim of the present study is to investigate the effects of Nix on mitophagy and mitochondrial function in airway epithelial cells exposed to cigarette smoke extract (CSE). Our present study has found that CSE could increase Nix protein expression and induce mitophagy in airway epithelial cells. And Nix siRNA significantly inhibited mitophagy and attenuated mitochondrial dysfunction and cell injury when airway epithelial cells were stimulated with 7.5% CSE. In contrast, Nix overexpression enhanced mitophagy and aggravated mitochondrial dysfunction and cell injury when airway epithelial cells were incubated with 7.5% CSE. These data suggest that Nix‐dependent mitophagy promotes airway epithelial cell and mitochondria injury induced by cigarette smoke, and may be involved in the pathogenesis of COPD and other cigarette smoke‐associated diseases. CSE increased Nix protein expression and induced mitophagy in Beas‐2b cells. Nix siRNA attenuated mitophagy, mitochondrial dysfunction, and cell injury induced by 7.5% CSE. Nix overexpression could enhance mitophagy and aggravate mitochondria and cell injury when airway epithelial cells were stimulated with 7.5% CSE.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 0021-9541eISSN: 1097-4652DOI: 10.1002/jcp.28117Titel-ID: cdi_proquest_journals_2211498671
- Format
- –
- Schlagworte
- airway epithelial cell, Autophagy, Bronchi - injuries, Bronchi - metabolism, Bronchi - pathology, Cell injury, Cell Line, Chronic obstructive pulmonary disease, Cigarette smoke, cigarette smoke extract, Cigarette Smoking - adverse effects, Cigarettes, Epithelial cells, Epithelial Cells - drug effects, Epithelial Cells - pathology, Epithelial Cells - ultrastructure, Gene Expression Regulation - genetics, Humans, Injuries, Lung diseases, Lung Injury - chemically induced, Lung Injury - genetics, Lung Injury - pathology, Membrane Proteins - genetics, Microscopy, Electron, Transmission, Mitochondria, Mitochondria - drug effects, Mitochondria - genetics, mitochondrial dysfunction, Mitophagy, Mitophagy - drug effects, Mitophagy - genetics, Mucous membrane, Nicotiana - adverse effects, Nix, Obstructive lung disease, Pathogenesis, Phagocytosis, Proteins, Proto-Oncogene Proteins - genetics, Pulmonary Disease, Chronic Obstructive - chemically induced, Pulmonary Disease, Chronic Obstructive - genetics, Pulmonary Disease, Chronic Obstructive - pathology, Respiratory tract, RNA, Small Interfering - genetics, RNA, Small Interfering - pharmacology, Signal Transduction - genetics, siRNA, Smoke, Tobacco smoke, Tumor Suppressor Proteins - genetics