Prolonged cigarette smoke exposure alters mitochondrial structure and function in airway epithelial cells
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- 作者：Roland F Hoffmann (1) (4)
Sina Zarrintan (2) (3)
Simone M Brandenburg (1)
Arjan Kol (1)
Harold G de Bruin (1) (4)
Shabnam Jafari (3)
Freark Dijk (3)
Dharamdajal Kalicharan (3)
Marco Kelders (6)
Harry R Gosker (6)
Nick HT ten Hacken (4) (5)
Johannes J van der Want (3) (7)
Antoon JM van Oosterhout (1) (4)
Irene H Heijink (1) (4) (5) - 关键词：Mitochondria ; Primary bronchial epithelial cells ; Smoking ; Reactive oxygen species ; COPD
- 刊名：Respiratory Research
- 出版年：2013
- 出版时间：December 2013
- 年：2013
- 卷：14
- 期：1
- 全文大小：1,212 KB
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51. Lo Tam Loi AT, Hoonhorst SJM, Franciosi L, Bischoff R, Hoffmann RF, Heijink I, / et al.: Acute and chronic inflammatory responses induced by smoking in individuals susceptible and non-susceptible to development of COPD: from specific disease phenotyping towards novel therapy. Protocol of a cross-sectional study. / BMJ Open 2013,3(2):e002178. mjopen-2012-002178" target="_blank" title="It opens in new window">CrossRef - 作者单位：Roland F Hoffmann (1) (4)
Sina Zarrintan (2) (3)
Simone M Brandenburg (1)
Arjan Kol (1)
Harold G de Bruin (1) (4)
Shabnam Jafari (3)
Freark Dijk (3)
Dharamdajal Kalicharan (3)
Marco Kelders (6)
Harry R Gosker (6)
Nick HT ten Hacken (4) (5)
Johannes J van der Want (3) (7)
Antoon JM van Oosterhout (1) (4)
Irene H Heijink (1) (4) (5)
1. Department of Pathology and Medical Biology, Laboratory of Allergology and Pulmonary Diseases, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
4. GRIAC Research Institute, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
2. Department of General Surgery, Tabriz University of Medical Sciences, Tabriz, Iran
3. Department of Cell Biology, Groningen University, University Medical Center Groningen, Groningen, The Netherlands
6. Department of Respiratory Medicine, NUTRIM School for Nutrition, Toxicology and Metabolism, Maastricht University Medical Center+, Maastricht, The Netherlands
5. Department of Pulmonology, University of Groningen, University Medical Center Groningen, Groningen, The Netherlands
7. Department of Laboratory Medicine, Electron Microscopy and Histology, Children’s and Women’s Health, Norwegian University of Science and Technology, Trondheim, Norway - ISSN：1465-9921
文摘
Background Cigarette smoking is the major risk factor for COPD, leading to chronic airway inflammation. We hypothesized that cigarette smoke induces structural and functional changes of airway epithelial mitochondria, with important implications for lung inflammation and COPD pathogenesis. Methods We studied changes in mitochondrial morphology and in expression of markers for mitochondrial capacity, damage/biogenesis and fission/fusion in the human bronchial epithelial cell line BEAS-2B upon 6-months from ex-smoking COPD GOLD stage IV patients to age-matched smoking and never-smoking controls. Results We observed that long-term CSE exposure induces robust changes in mitochondrial structure, including fragmentation, branching and quantity of cristae. The majority of these changes were persistent upon CSE depletion. Furthermore, long-term CSE exposure significantly increased the expression of specific fission/fusion markers (Fis1, Mfn1, Mfn2, Drp1 and Opa1), oxidative phosphorylation (OXPHOS) proteins (Complex II, III and V), and oxidative stress (Mn-SOD) markers. These changes were accompanied by increased levels of the pro-inflammatory mediators IL-6, IL-8, and IL-1β. Importantly, COPD primary bronchial epithelial cells (PBECs) displayed similar changes in mitochondrial morphology as observed in long-term CSE-exposure BEAS-2B cells. Moreover, expression of specific OXPHOS proteins was higher in PBECs from COPD patients than control smokers, as was the expression of mitochondrial stress marker PINK1. Conclusion The observed mitochondrial changes in COPD epithelium are potentially the consequence of long-term exposure to cigarette smoke, leading to impaired mitochondrial function and may play a role in the pathogenesis of COPD.