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Nix/BNIP3L‐dependent mitophagy accounts for airway epithelial cell injury induced by cigarette smoke
Author(s) -
Zhang Ming,
Shi Rong,
Zhang Yeli,
Shan Hu,
Zhang Qiuhong,
Yang Xia,
Li Yali,
Zhang Jie
Publication year - 2019
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.28117
Subject(s) - mitophagy , autophagy , copd , mitochondrion , microbiology and biotechnology , pathogenesis , cigarette smoke , airway , cell , cancer research , medicine , immunology , chemistry , biology , apoptosis , biochemistry , surgery , environmental health
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.