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Identification of apoptosis‐associated protein factors distinctly expressed in cigarette smoke condensate‐exposed airway bronchial epithelial cells
Author(s) -
Lin Bencheng,
Li Qiuyue,
Tian Lei,
Liu Huanliang,
Liu Xiaohua,
Shi Yue,
He Chen,
Ding Susu,
Yan Jun,
Li Kang,
Bian Liping,
Lai Wenqing,
Zhang Wei,
Li Xiang,
Xi Zhuge
Publication year - 2020
Publication title -
journal of biochemical and molecular toxicology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.526
H-Index - 58
eISSN - 1099-0461
pISSN - 1095-6670
DOI - 10.1002/jbt.22444
Subject(s) - apoptosis , cancer research , tumor necrosis factor alpha , receptor , immunology , cell , oxidative stress , lung cancer , respiratory epithelium , tobacco smoke , asthma , biology , medicine , chemistry , microbiology and biotechnology , epithelium , pathology , endocrinology , biochemistry , environmental health
Smoking is associated with an increased risk of respiratory diseases, including lung cancer and asthma. However, the mechanisms or diagnostic markers for smoking‐related diseases remain largely unknown. Here we investigated the role of cigarette smoke condensate (CSC) in the regulation of human bronchial epithelial cell (BEAS‐2B) behavior. We found that exposure to CSC significantly inhibited BEAS‐2B cell viability, impaired cell morphology, induced cell apoptosis, triggered oxidative damage, and promoted inflammatory response, which suggests a deleterious effect of CSC on bronchial epithelial cells. In addition, CSC markedly altered the expression of apoptosis‐associated protein factors, including p21, soluble tumor necrosis factor receptor 1, and Fas ligand. In sum, our study identified a panel of novel protein factors that may mediate the actions of CSC on bronchial epithelial cells and have a predictive value for the development and progression of smoking‐related diseases, thus providing insights into the development of potential diagnostic and therapeutic strategies against these diseases.