Cyclophilin D Contributes to Airway Epithelial Mitochondrial Damage in Chronic Obstructive Pulmonary Disease

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Published in:Lung. - Springer US, 1903. - 201(2023), 3 vom: 01. Juni, Seite 287-295
Main Author: Zhang, Rui (Author)
Other Authors: Shan, Hu (Author) Li, Yuer (Author) Ma, Yuefeng (Author) Liu, Shiyuan (Author) Liu, Xiaohuan (Author) Yang, Xia (Author) Zhang, Jie (Author) Zhang, Ming (Author)
Format: electronic Article
Language:English
Published: 2023
ISSN:1432-1750
External Sources:lizenzpflichtig
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500 |a © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. 
520 |a Introduction Airway epithelial mitochondrial injury is an important pathogenesis of chronic obstructive pulmonary disease (COPD). Cyclophilin D (CypD) is a component of mitochondrial permeability transition pore and related to mitochondrial damage. However, the role of CypD in airway epithelial mitochondrial injury and COPD pathogenesis remains unclear. Methods CypD expression in human airway epithelium was determined by immunohistochemistry, and mitochondrial structure of airway epithelial cell was observed under the transmission electron microscopy. The expression of CypD signaling pathway in cigarette smoke extract (CSE)-treated airway epithelial cells was measured by real-time PCR and Western-blot. CSE-induced damage of airway epithelial cell and mitochondria was further studied. Results Immunohistochemistry and transmission electron microscopy analysis revealed that CypD expression in airway epithelium was significantly increased associated with notable airway epithelial mitochondrial structure damage in the patients with COPD. The mRNA and protein expression of CypD was significantly increased in concentration- and time-dependent manners when airway epithelial cells were treated with CSE. CypD siRNA pretreatment significantly suppressed the increases of CypD and Bax expression, and reduced the decline of Bcl-2 expression in 7.5% CSE-treated airway epithelial cells. Furthermore, CypD silencing significantly attenuated mitochondrial damage and cell apoptosis, and increased cell viability when airway epithelial cells were stimulated with 7.5% CSE. Conclusion These data suggest that CypD signaling pathway is involved in the pathogenesis of COPD and provide a potential therapeutic target for COPD. 
650 4 |a Cyclophilin D 
650 4 |a Mitochondria 
650 4 |a Airway epithelial cell 
650 4 |a Cigarette smoke extract 
650 4 |a Chronic obstructive pulmonary disease 
700 1 |a Shan, Hu  |4 aut 
700 1 |a Li, Yuer  |4 aut 
700 1 |a Ma, Yuefeng  |4 aut 
700 1 |a Liu, Shiyuan  |4 aut 
700 1 |a Liu, Xiaohuan  |4 aut 
700 1 |a Yang, Xia  |4 aut 
700 1 |a Zhang, Jie  |4 aut 
700 1 |a Zhang, Ming  |4 aut 
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