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Therefore, we hypothesized that the \u03b2-agonist isoproterenol would affect wound healing. Using an in vitro scrape wound assay, we demonstrated that isoproterenol attenuates EGF-stimulated wound healing in 16HBE airway epithelial cell cultures. Through experiments with forskolin and cells overexpressing \u03b2<jats:sub>2<\/jats:sub>-adrenergic receptor-yellow fluorescent protein, we show that attenuation is due to the accumulation of cAMP and the involvement of at least one additional pathway. Furthermore, attenuation is not due to a direct effect on the EGF receptor or to an alteration of the ERK\/MAPK signaling cascade. Based on these results, we propose that isoproterenol may exert its effects through other MAPK signaling pathways (JNK and\/or p38) or through parallel mechanisms. These results also demonstrate a problem of potential therapeutic relevance in which a commonly prescribed medication may alter wound healing and contribute to the remodeling of asthmatic airways.<\/jats:p>","DOI":"10.1152\/ajplung.00233.2005","type":"journal-article","created":{"date-parts":[[2005,10,15]],"date-time":"2005-10-15T00:24:16Z","timestamp":1129335856000},"page":"L485-L491","source":"Crossref","is-referenced-by-count":9,"title":["The \u03b2-agonist isoproterenol attenuates EGF-stimulated wound closure in human airway epithelial cells"],"prefix":"10.1152","volume":"290","author":[{"given":"Bradley J.","family":"Schnackenberg","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Stacie 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