单位：[1]The Center for Biomedical Research, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Caidian 431000, China华中科技大学同济医学院附属同济医院生物医学研究中心生物医学中心科研平台[2]Department of Respiratory and Critical Care Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China华中科技大学同济医学院附属同济医院内科学系呼吸与危重症医学科[3]The Technology Center, China Tobacco Jiangxi Industrial Co., Ltd., Nanchang High Technology Development Valley, Nanchang 330096, China.
BackgroundChronic obstructive pulmonary disease (COPD) characterized by the airway and lung inflammation, is a leading cause of morbidity and mortality worldwide, especially among smokers over 40years of age and individuals exposed to biomass smoke. Although the detailed mechanisms of this disease remain elusive, there is feasible evidence that protein posttranslational modifications (PTMs) may play a role in its pathoetiology. We thus conducted studies to dissect the effect of cigarette smoke extracts (CSE) on the change of SUMOylated substrates in human bronchial epithelial cells (HBEs).MethodsSamples were collected in HBEs with or without 24h of CSE insult and then subjected to Western-blot and LC-MS/MS analysis. Subsequently, bioinformatic tools were used to analyze the data. The effect of SUMOylation on cytochrome P450 1A1 (CYP1A1) was evaluated by flow cytometry.ResultsIt was noted that CSE stimulated HBEs to undergo a SUMOylation turnover as evidenced by the changes of SUMOylated substrates and SUMOylation levels for a particular substrate. The SUMOylated proteins are relevant to the regulation of biological processes, molecular function and cellular components. Particularly, CSE stimulated a significant increase of SUMOylated CYP1A1, a critical enzyme involved in the induction of oxidative stress.ConclusionsOur data provide a protein SUMOylation profile for better understanding of the mechanisms underlying COPD and support that smoking induces oxidative stress in HBEs, which may predispose to the development of COPD in clinical settings.
基金：
Integrated Innovative Team for Major Human Disease Programs of Tongji Medical College, Huazhong University of Science and Technology; Innovative Funding for Translational Research from Tongji Hospital
第一作者单位：[1]The Center for Biomedical Research, Tongji Hospital Research Building, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, Caidian 431000, China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
zhou haifeng,zhang lei,li yang,et al.Cigarette smoke extract stimulates bronchial epithelial cells to undergo a SUMOylation turnover[J].BMC PULMONARY MEDICINE.2020,20(1):doi:10.1186/s12890-020-01300-w.
APA：
zhou,haifeng,zhang,lei,li,yang,wu,guorao,zhu,he...&wang,cong-yi.(2020).Cigarette smoke extract stimulates bronchial epithelial cells to undergo a SUMOylation turnover.BMC PULMONARY MEDICINE,20,(1)
MLA：
zhou,haifeng,et al."Cigarette smoke extract stimulates bronchial epithelial cells to undergo a SUMOylation turnover".BMC PULMONARY MEDICINE 20..1(2020)
