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Upregulation of CTGF in this in vitro model was independent of TGF-\u03b2 secreted into the growth medium. Comparison of E1A-positive with E1A-negative HBE cells showed that both expressed cytokeratin but only E1A-positive cells expressed the mesenchymal markers vimentin and \u03b1-smooth muscle actin. We conclude that latent infection of epithelial cells by adenovirus E1A could contribute to airway remodeling in COPD by the viral E1A gene, inducing TGF-\u03b21 and CTGF expression and shifting cells to a more mesenchymal phenotype.<\/jats:p>","DOI":"10.1152\/ajplung.00315.2002","type":"journal-article","created":{"date-parts":[[2004,1,31]],"date-time":"2004-01-31T00:55:58Z","timestamp":1075510558000},"page":"L189-L197","source":"Crossref","is-referenced-by-count":27,"title":["Latent adenoviral infection induces production of growth factors relevant to airway remodeling in COPD"],"prefix":"10.1152","volume":"286","author":[{"given":"Emiko","family":"Ogawa","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"W. 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