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This Article Full Text Full Text (PDF) All Versions of this Article: 291/1/L84    most recent 00388.2005v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via ISI Web of Science (7) Citing Articles via Google Scholar Google Scholar Articles by Lee, S. Y. Articles by Shim, J. J. Search for Related Content PubMed PubMed Citation Articles by Lee, S. Y. Articles by Shim, J. J.

Peroxisome proliferator-activated receptor- inhibits cigarette smoke solution-induced mucin production in human airway epithelial (NCI-H292) cells

¹Department of Internal Medicine, Guro Hospital, Korea University, Seoul; ²Department of Internal Medicine, Anam Hospital, Korea University, Seoul; and ³Department of Internal Medicine, Ansan Hospital, Korea University, Ansan, Korea

Submitted 9 September 2005 ; accepted in final form 16 January 2006

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- (PPAR-) is a member of the ligand-activated nuclear receptor superfamily. PPAR- is implicated in anti-inflammatory responses, but mechanisms underlying these varied roles remain ill-defined. Recently, reports have shown that upregulation of phosphatase and tensin homolog deleted on chromosome 10 (PTEN) might be one of the mechanisms through which PPAR- agonists exert their anti-inflammatory actions. However, no data are available on the role of PPAR- in smoke-induced mucin production. In this study, we investigated the effect of PPAR- agonist (rosiglitazone) on smoke-induced mucin production in NCI-H292 cells. Exposure to cigarette smoke causes a significant decrease in PTEN expression and increases dose-dependent EGFR-specific tyrosine phosphorylation, resulting in MUC5AC mucin production in NCI-H292 cells. PPAR- agonists or specific inhibitors of phosphoinositide 3-kinase exert inhibition of cigarette smoke-induced mucin production, with the upregulation of PTEN signaling and downregulation of Akt expression. This study demonstrates that PPAR- agonist functions as a regulator of epithelial cell inflammation that may result in reduction of mucin-producing cells in airway epithelium.

rosiglitazone; epidermal growth factor receptor; phosphatase and tensin homolog deleted on chromosome 10; smoking

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