HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) All Versions of this Article: 286/1/L189    most recent 00315.2002v1 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 Web of Science 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 Web of Science (14) Citing Articles via Google Scholar Google Scholar Articles by Ogawa, E. Articles by Hayashi, S. Search for Related Content PubMed PubMed Citation Articles by Ogawa, E. Articles by Hayashi, S.

Latent adenoviral infection induces production of growth factors relevant to airway remodeling in COPD

¹McDonald Research Laboratories-iCAPTURE Centre, Department of Pathology and Laboratory Medicine, St. Paul's Hospital-Providence Health Care, University of British Columbia, Vancouver, British Columbia, Canada V6Z 1Y6; and ²RA Biology and ³Asthma Disease Biology, GlaxoSmithKline R&D, Stevenage SG1 2NY, United Kingdom

Submitted 17 September 2002 ; accepted in final form 22 September 2003

Previous studies showed an association between latent adenoviral infection with expression of the adenoviral E1A gene and chronic obstructive pulmonary disease (COPD). The present study focuses on how the adenoviral E1A gene could alter expression of growth factors by human bronchial epithelial (HBE) cells. The data show that connective tissue growth factor (CTGF) and transforming growth factor (TGF)-1 mRNA and protein expression were upregulated in E1A-positive HBE cells. Upregulation of CTGF in this in vitro model was independent of TGF- 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 -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-1 and CTGF expression and shifting cells to a more mesenchymal phenotype.

bronchial epithelial cell; differentiation; transforming growth factor-; connective tissue growth factor; chronic obstructive pulmonary disease

This article has been cited by other articles:

				S. Sethi, P. Mallia, and S. L. Johnston New Paradigms in the Pathogenesis of Chronic Obstructive Pulmonary Disease II Proceedings of the ATS, September 15, 2009; 6(6): 532 - 534. [Abstract] [Full Text] [PDF]

				K. Morimoto, J. Gosselink, A. Kartono, J. C. Hogg, S. Hayashi, and E. Ogawa Adenovirus E1A regulates lung epithelial ICAM-1 expression by interacting with transcriptional regulators at its promoter Am J Physiol Lung Cell Mol Physiol, March 1, 2009; 296(3): L361 - L371. [Abstract] [Full Text] [PDF]

				R. Lutter and M. Spiteri Current perspectives in epithelial cell injury and repair: consequences for epithelial functions Eur. Respir. Rev., December 1, 2005; 14(97): 126 - 130. [Abstract] [Full Text] [PDF]

				A. Dorn, H. Zhao, F. Granberg, M. Hosel, D. Webb, C. Svensson, U. Pettersson, and W. Doerfler Identification of Specific Cellular Genes Up-Regulated Late in Adenovirus Type 12 Infection J. Virol., February 15, 2005; 79(4): 2404 - 2412. [Abstract] [Full Text] [PDF]