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Sirtuin 3 Inhibits Airway Epithelial Mitochondrial Oxidative Stress in Cigarette Smoke-Induced COPD.
Oxid Med Cell Longev. 2020; 2020:7582980.OM

Abstract

Mitochondrial damage in airway epithelial cells plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Sirtuin 3 (Sirt3) is a mitochondrial deacetylase regulating mitochondrial function, but its role in the pathogenesis of COPD is still unknown. The aim of the present study was to investigate the effect of Sirt3 on airway epithelial mitochondria in cigarette smoke-induced COPD. Our present study has shown serious airway inflammation, alveolar space enlargement, and mitochondrial damage of the airway epithelium in COPD rats. Compared to the control rats, Sirt3 protein expression was significantly decreased in the airway epithelium and lung tissue homogenate from COPD rats. In airway epithelial cells (BEAS-2B), cigarette smoke extract (CSE) treatment significantly decreased mRNA and protein expression of Sirt3 and manganese superoxide dismutase (MnSOD), as well as MnSOD activity in a concentration and time-dependent manner. Sirt3 siRNA further significantly intensified the decreases in MnSOD expression and activity and aggravated mitochondrial oxidative stress and cell injury when airway epithelial cells were treated with 7.5% CSE. In contrast, Sirt3 overexpression significantly prevented the decrease of MnSOD expression and activity and improved mitochondrial oxidative stress and cell injury in CSE-treated airway epithelial cells. These data suggest that Sirt3 inhibits airway epithelial mitochondrial oxidative stress possibly through the regulation of MnSOD, thereby contributing to the pathogenesis of COPD.

Authors+Show Affiliations

Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.Pulmonary Cell Research & Clinic of Respiratory Medicine, Dept. Biomedicine University of Basel & University Hospital of Basel, CH-4031 Basel, Switzerland.Department of Urology, The Ninth Hospital of Xi'an, Xi'an, Shaanxi, China.Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.Department of Respiratory and Critical Care Medicine, The Second Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

33005288

Citation

Zhang, Ming, et al. "Sirtuin 3 Inhibits Airway Epithelial Mitochondrial Oxidative Stress in Cigarette Smoke-Induced COPD." Oxidative Medicine and Cellular Longevity, vol. 2020, 2020, p. 7582980.
Zhang M, Zhang Y, Roth M, et al. Sirtuin 3 Inhibits Airway Epithelial Mitochondrial Oxidative Stress in Cigarette Smoke-Induced COPD. Oxid Med Cell Longev. 2020;2020:7582980.
Zhang, M., Zhang, Y., Roth, M., Zhang, L., Shi, R., Yang, X., Li, Y., & Zhang, J. (2020). Sirtuin 3 Inhibits Airway Epithelial Mitochondrial Oxidative Stress in Cigarette Smoke-Induced COPD. Oxidative Medicine and Cellular Longevity, 2020, 7582980. https://doi.org/10.1155/2020/7582980
Zhang M, et al. Sirtuin 3 Inhibits Airway Epithelial Mitochondrial Oxidative Stress in Cigarette Smoke-Induced COPD. Oxid Med Cell Longev. 2020;2020:7582980. PubMed PMID: 33005288.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Sirtuin 3 Inhibits Airway Epithelial Mitochondrial Oxidative Stress in Cigarette Smoke-Induced COPD. AU - Zhang,Ming, AU - Zhang,Yeli, AU - Roth,Michael, AU - Zhang,Li, AU - Shi,Rong, AU - Yang,Xia, AU - Li,Yali, AU - Zhang,Jie, Y1 - 2020/09/11/ PY - 2020/06/18/received PY - 2020/08/24/revised PY - 2020/08/27/accepted PY - 2020/10/2/entrez PY - 2020/10/3/pubmed PY - 2021/5/13/medline SP - 7582980 EP - 7582980 JF - Oxidative medicine and cellular longevity JO - Oxid Med Cell Longev VL - 2020 N2 - Mitochondrial damage in airway epithelial cells plays an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD). Sirtuin 3 (Sirt3) is a mitochondrial deacetylase regulating mitochondrial function, but its role in the pathogenesis of COPD is still unknown. The aim of the present study was to investigate the effect of Sirt3 on airway epithelial mitochondria in cigarette smoke-induced COPD. Our present study has shown serious airway inflammation, alveolar space enlargement, and mitochondrial damage of the airway epithelium in COPD rats. Compared to the control rats, Sirt3 protein expression was significantly decreased in the airway epithelium and lung tissue homogenate from COPD rats. In airway epithelial cells (BEAS-2B), cigarette smoke extract (CSE) treatment significantly decreased mRNA and protein expression of Sirt3 and manganese superoxide dismutase (MnSOD), as well as MnSOD activity in a concentration and time-dependent manner. Sirt3 siRNA further significantly intensified the decreases in MnSOD expression and activity and aggravated mitochondrial oxidative stress and cell injury when airway epithelial cells were treated with 7.5% CSE. In contrast, Sirt3 overexpression significantly prevented the decrease of MnSOD expression and activity and improved mitochondrial oxidative stress and cell injury in CSE-treated airway epithelial cells. These data suggest that Sirt3 inhibits airway epithelial mitochondrial oxidative stress possibly through the regulation of MnSOD, thereby contributing to the pathogenesis of COPD. SN - 1942-0994 UR - https://www.unboundmedicine.com/medline/citation/33005288/Sirtuin_3_Inhibits_Airway_Epithelial_Mitochondrial_Oxidative_Stress_in_Cigarette_Smoke_Induced_COPD_ DB - PRIME DP - Unbound Medicine ER -