beta-Catenin is not necessary for maintenance or repair of the bronchiolar epithelium.


Journal Article

Signaling by Wnt/beta-catenin regulates self-renewal of tissue stem cells in the gut and, when activated in the embryonic bronchiolar epithelium, leads to stem cell expansion. We have used transgenic and cell type-specific knockout strategies to determine roles for beta-catenin-regulated gene expression in normal maintenance and repair of the bronchiolar epithelium. Analysis of TOPGal transgene activity detected beta-catenin signaling in the steady-state and repairing bronchiolar epithelium. However, the broad distribution and phenotype of signaling cells precluded establishment of a clear role for beta-catenin in the normal or repairing state. Necessity of beta-catenin signaling was tested through Cre-mediated deletion of Catnb exons 2-6 in airway epithelial cells. Functional knockout of beta-catenin had no impact on expression of Clara cell differentiation markers, mitotic index, or sensitivity of these cells to the Clara cell-specific toxicant, naphthalene. Repair of the naphthalene-injured airway proceeded with establishment of focal regions of beta-catenin-null epithelium. The size of regenerative epithelial units, mitotic index, and restoration of the ciliated cell population did not vary between wild-type and genetically modified mice. Thus, beta-catenin was not necessary for maintenance or efficient repair of the bronchiolar epithelium.

Full Text

Duke Authors

Cited Authors

  • Zemke, AC; Teisanu, RM; Giangreco, A; Drake, JA; Brockway, BL; Reynolds, SD; Stripp, BR

Published Date

  • November 2009

Published In

Volume / Issue

  • 41 / 5

Start / End Page

  • 535 - 543

PubMed ID

  • 19213872

Pubmed Central ID

  • 19213872

Electronic International Standard Serial Number (EISSN)

  • 1535-4989

Digital Object Identifier (DOI)

  • 10.1165/rcmb.2008-0407OC


  • eng

Conference Location

  • United States