Overexpression of Forkhead box C1 attenuates oxidative stress, inflammation and apoptosis in chronic obstructive pulmonary disease

Publication date: Available online 11 November 2018Source: Life SciencesAuthor(s): Shuyue Xia, Jian Qu, Hui Jia, Wei He, Jing Li, Long Zhao, Mingqing Mao, Yan ZhaoAbstractAimChronic obstructive pulmonary disease (COPD) is a disease caused by cigarette smoke, which has been emerging as a serious health problem worldwide. The aim of this study is to explore the mRNA expression profile of lung tissues from the COPD rats and to characterize the role of Forkhead box C1 (Foxc1) in COPD.Main methodsWistar rats were exposed to cigarette smoke during 16 weeks for COPD model establishment. The microarray was used to identify the differential gene expression in the lung of rats. Adenovirus carrying Foxc1 was administered to rats by intratracheally instillation once a week for 16 weeks. Human bronchial epithelial cell line (16HBE) cells were transfected with Foxc1 siRNA followed by incubation in the presence of CSE (10%) for 24 h. Subsequently, the pathological changes, fibrosis, apoptosis, inflammatory cytokines and oxidative stress were detected.Key findingsMicroarray results showed an upregulation of Foxc1 in lung tissues in COPD rats. Overexpression of Foxc1 mitigated the lung injury, as evidenced by reducing alveolar fusion, inflammatory cell infiltration and oxidative stress. Additionally, the apoptosis was remarkably increased in the lung in rats exposed to cigarette smoke, which was suppressed by Foxc1 overexpression. Furthermore, downregulation of Foxc1 aggravated the infl...
Source: Life Sciences - Category: Biology Source Type: research