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Published ahead of print on October 5, 2007, doi:10.1165/rcmb.2007-0182OC

Am. J. Respir. Cell Mol. Biol., Volume 38, Number 3, March 2008, 337-345

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Submitted on May 21, 2007
Revised on October 5, 2007

Conditional Deletion of Pten Causes Bronchiolar Hyperplasia

Vrushank Dave'1*, Susan E Wert1, Tiffany Tanner1, Angela R Thitoff1, Dave E Loudy1, and Jeffrey A Whitsett1

1 Division of Pulmonary, Neonatology and Perinatal Biology, Cincinnati Children's Hospital Medical Center, University of Cincinnati College of Medicine, Cincinnati, Ohio, USA

* To whom correspondence should be addressed. E-mail: davev0{at}cchmc.org.

Tumor suppressor phosphatase and tensin homologue deleted on chromosome 10 (PTEN) is a lipid phosphatase that regulates multiple cellular processes including cell polarity, migration, proliferation and carcinogenesis. In this work, we demonstrate that conditional deletion of Pten (Pten{Delta}/{Delta}) in the respiratory epithelial cell proliferation and hyperplasia as early as 4-6 weeks of age. While bronchiolar cell differentiation was normal, as indicated by {beta}-tubulin and FOXJ1 expression in ciliated cells and, CCSP expression in non-ciliated cells; cell proliferation, detected by expression of Ki-67, phospho-histone-H3 and cyclin D1, was increased and associated with activation of the AKT/mTOR survival pathway. Deletion of Pten caused papillary epithelial hyperplasia characterized by a hypercellular epithelium lining papillae with fibrovascular cores that protruded into the airway lumens. Cell polarity, as assessed by sub-cellular localization of cadherin, {beta}-catenin and ZO-1, was unaltered. PTEN is required for regulation of epithelial cell proliferation in the lung and for the maintenance of the normal simple columnar epithelium characteristics of bronchi and bronchioles.




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