| First Author | Davé V | Year | 2008 |
| Journal | Am J Respir Cell Mol Biol | Volume | 38 |
| Issue | 3 | Pages | 337-45 |
| PubMed ID | 17921358 | Mgi Jnum | J:146355 |
| Mgi Id | MGI:3837301 | Doi | 10.1165/rcmb.2007-0182OC |
| Citation | Dave V, et al. (2008) Conditional deletion of Pten causes bronchiolar hyperplasia. Am J Respir Cell Mol Biol 38(3):337-45 |
| abstractText | Tumor suppressor phosphatase and tensin homolog 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 cells of the developing mouse lung caused epithelial cell proliferation and hyperplasia as early as 4 to 6 weeks of age. While bronchiolar cell differentiation was normal, as indicated by beta-tubulin and FOXJ1 expression in ciliated cells and by CCSP expression in nonciliated 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 subcellular localization of cadherin, beta-catenin, and zonula occludens-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. |
