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Published ahead of print on August 27, 2004, doi:10.1165/rcmb.2004-0092OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 6, December 2004, 650-656

A more recent version of this article appeared on December 1, 2004
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Submitted on March 15, 2004
Revised on August 26, 2004

Conditional overexpression of bioactive TGF-{beta}1 in neonatal mouse lung: A new model for BPD?

Alfin G Vicencio, Chun Geun Lee, Soo Jung Cho1, Oliver Eickelberg2, Ying Chuu3, Gabriel G Haddad3, and Jack A Elias1*

1 Department of Internal Medicine, Yale University School of Medicine, New Haven, CT, USA, 2 Department of Internal Medicine, Giessen University School of Medicine, Giessen, Germany, 3 Department of Pediatrics, Albert Einstein College of Medicine and Children's Hospital at Montefiore, Bronx, NY, USA

* To whom correspondence should be addressed. E-mail: jack.elias{at}yale.edu.

Research interest in bronchopulmonary dysplasia (BPD) has steadily increased, and numerous potential mediators have been implicated in the development of the disease. Among such mediators is transforming growth factor-{beta} (TGF-{beta}). Unfortunately, commonly utilized murine transgenic models are not optimal to investigate the effects of TGF-{beta} specifically during the 2-3 week period of alveolar formation, the developmental stage that corresponds histologically to early alveolar development in humans, and the time frame during which BPD develops. In the current study, we utilize a triple-transgenic construct to overexpress bioactive TGF-{beta}1 in the neonatal mouse lung during the period of alveolar formation. Lungs were then examined by histologic, western blot and immunofluorescent methods. We found that overexpression of bioactive TGF-{beta}1 in neonatal mouse lungs resulted in structural changes that have been described in BPD. Included in those characteristics are abnormal alveolar structure, cellular composition and vascular development. Our study indicates that TGF-{beta}1 overexpression in the neonatal mouse lung results in histologic alterations that have striking similarities to pathologic descriptions of BPD. We encourage the use of conditional transgenic models for the study of BPD and hypothesize that the TGF-{beta} system is a central mediator for the histologic alterations described in the disease.




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