Deletion of Pten expands lung epithelial progenitor pools and confers resistance to airway injury.

ABSTRACT:

Rationale

Pten is a tumor-suppressor gene involved in stem cell homeostasis and tumorigenesis. In mouse, Pten expression is ubiquitous and begins as early as 7 days of gestation. Pten(-/-) mouse embryos die early during gestation indicating a critical role for Pten in embryonic development.

Objectives

To test the role of Pten in lung development and injury.

Methods

We conditionally deleted Pten throughout the lung epithelium by crossing Pten(flox/flox) with Nkx2.1-cre driver mice. The resulting Pten(Nkx2.1-cre) mutants were analyzed for lung defects and response to injury.

Measurements and main results

Pten(Nkx2.1-cre) embryonic lungs showed airway epithelial hyperplasia with no branching abnormalities. In adult mice, Pten(Nkx2.1-cre) lungs exhibit increased pr

SUBMITTER: Tiozzo C 

PROVIDER: S-EPMC2778148 | biostudies-literature | 2009 Oct

REPOSITORIES: biostudies-literature