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Published online before print May 17, 2006
Eur Respir J 2006, doi:10.1183/09031936.06.00078405
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ORIGINAL ARTICLE

Altered expression of the Smad signalling pathway: implications for COPD pathogenesis

A. Zandvoort 1, D.S. Postma 2, M.R. Jonker 3, J.A. Noordhoek 2, J.T.W.M. Vos 3, Y.M. van der Geld 3, W. Timens 3*

1 Depts of Pathology and Laboratory Medicine; and Pulmonology, University Medical Center Groningen, University of Groningen, The Netherlands
2 Pulmonology, University Medical Center Groningen, University of Groningen, The Netherlands
3 Depts of Pathology and Laboratory Medicine

* To whom correspondence should be addressed. E-mail: w.timens{at}path.umcg.nl.


  Abstract

Pulmonary emphysema, as a feature of COPD, is characterized by destruction of alveolar tissue. We previously demonstrated reduced decorin expression in the peribronchial area of COPD patients reflecting an altered ECM modulation. Decorin transcription is regulated by the TGF{beta}-Smad pathway, the key intracellular signal route for initiation of ECM component gene transcription. Whether this pathway is aberrantly expressed in COPD is not known.

An immunohistochemical study was performed to compare protein expression of TGF{beta}-1, TGF{beta} receptors, Smad 2, 3, 4, 7, and decorin in lung tissue of GOLD stage II and stage IV COPD patients and controls.

Epithelial expression of the inhibitory Smad 7 was significantly lower in patients with GOLD stage II and with stage IV than in controls, other Smad protein expressions being similar in the groups. TGF{beta}-1 and TGF{beta} receptor type I were significantly lower expressed in stage II patients. Decorin staining of the adventitia and alveolar walls was significantly reduced in COPD stage IV.

We conclude that the TGF{beta}-Smad pathway is aberrantly expressed in COPD patients, implying an abnormal tissue repair ultimately resulting in reduced decorin production. Our results contribute to better understanding of the pathogenesis of emphysema and the airway fibrosis observed in COPD patients.

Keywords:  COPD, emphysema, immunohistochemistry, Smad, TGF{beta}-1, TNF{alpha}




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