References
Query Results -- Details
MGI Accession ID: MGI:3837301
J Number: J:146355
Other Accession IDs:
Title: Conditional deletion of Pten causes bronchiolar hyperplasia.
Authors: Dave V; Wert SE; Tanner T; Thitoff AR; Loudy DE; Whitsett JA
Journal: Am J Respir Cell Mol Biol
Volume: 38
Issue: 3
Date: 2008 Mar
Year: 2008
Pages: 337-45
Review Status: Peer Reviewed
Abstract:
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.
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