Shuyue Xia1, Jian Qu2, Hui Jia3, Wei He3, Jing Li2, Long Zhao3, Mingqing Mao3, Yan Zhao3. 1. Department of Respiratory and Critical Care Medicine, Central Hospital Affiliated to Shenyang Medical College, Shenyang 110024, People's Republic of China. Electronic address: Syx262@126.com. 2. Shenyang Environmental Monitor Central Station, Shenyang 110016, People's Republic of China. 3. Department of Respiratory and Critical Care Medicine, Central Hospital Affiliated to Shenyang Medical College, Shenyang 110024, People's Republic of China.
Abstract
AIM: Chronic 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 METHODS: Wistar 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 FINDINGS: Microarray 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 inflammation, oxidative stress and apoptosis in 16HBE cells with CSE treatment. SIGNIFICANCE: Overexpression of Foxc1 could prevent oxidative stress, inflammation responses and cell apoptosis and knockdown of Foxc1 has the opposite effect, suggesting that Foxc1 may be available for lung protection during COPD.
AIM: Chronic 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 COPDrats and to characterize the role of Forkhead box C1 (Foxc1) in COPD. MAIN METHODS:Wistar 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 FINDINGS: Microarray results showed an upregulation of Foxc1 in lung tissues in COPDrats. 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 inflammation, oxidative stress and apoptosis in 16HBE cells with CSE treatment. SIGNIFICANCE: Overexpression of Foxc1 could prevent oxidative stress, inflammation responses and cell apoptosis and knockdown of Foxc1 has the opposite effect, suggesting that Foxc1 may be available for lung protection during COPD.