Peroxisome proliferator-activated receptor- inhibits cigarette smoke solution- induced mucin production in human airway epithelial (NCI-H292) cells
نویسندگان
چکیده
Sung Yong Lee, Eun Joo Kang, Gyu Young Hur, Ki Hwan Jung, Hye Cheol Jung, Sang Yeub Lee, Je Hyeong Kim, Chol Shin, Kwang Ho In, Kyung Ho Kang, Se Hwa Yoo, and Jae Jeong Shim Department of Internal Medicine, Guro Hospital, Korea University, Seoul; Department of Internal Medicine, Anam Hospital, Korea University, Seoul; and Department of Internal Medicine, Ansan Hospital, Korea University, Ansan, Korea
منابع مشابه
Peroxisome proliferator-activated receptor-gamma inhibits cigarette smoke solution-induced mucin production in human airway epithelial (NCI-H292) cells.
The main etiologic factor for chronic bronchitis is cigarette smoke. Exposure to cigarette smoke is reported to induce goblet cell hyperplasia and mucus production. Mucin synthesis in airways has been reported to be regulated by the EGFR system. Peroxisome proliferator-activated receptor-gamma (PPAR-gamma) is a member of the ligand-activated nuclear receptor superfamily. PPAR-gamma is implicate...
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Shao, Matt X. G., Takashi Nakanaga, and Jay A. Nadel. Cigarette smoke induces MUC5AC mucin overproduction via tumor necrosis factor-converting enzyme in human airway epithelial (NCI-H292) cells. Am J Physiol Lung Cell Mol Physiol 287: L420– L427, 2004. First published April 30, 2004; 10.1152/ajplung. 00019.2004.—Chronic obstructive pulmonary disease (COPD) is one of the leading causes of death ...
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Pathogenic factors associated with chronic obstructive pulmonary disease (COPD), such as cigarette smoke, proinflammatory cytokines, and bacterial infections, can individually induce respiratory mucins in vitro and in vivo. Since co-presence of these factors is common in lungs of patients with COPD, we hypothesized that cigarette smoke can amplify mucin induction by bacterial exoproducts and pr...
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In the present study, we investigated whether apigenin significantly affects tumor necrosis factor-α (TNF-α)-induced production and gene expression of MUC5AC mucin in airway epithelial cells. Confluent NCI-H292 cells were pretreated with apigenin for 30 min and then stimulated with TNF-α for 24 h or the indicated periods. The MUC5AC mucin gene expression and mucin protein production were measur...
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