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

Anna C Zemke, Roxana M Teisanu, Adam Giangreco, Jeff A Drake, Brian L Brockway, Susan D Reynolds, Barry R Stripp

Research output: Contribution to journalArticlepeer-review

51 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)535-43
Number of pages9
JournalAmerican Journal of Respiratory Cell and Molecular Biology
Issue number5
Publication statusPrint publication - Nov 2009
Externally publishedYes


  • Animals
  • Bronchioles/drug effects
  • Cell Differentiation
  • Cell Proliferation
  • Gene Expression Regulation, Developmental
  • Gene Knockout Techniques
  • Integrases/genetics
  • Lac Operon
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Mitotic Index
  • Naphthalenes/toxicity
  • Phenotype
  • Promoter Regions, Genetic
  • RNA, Messenger/metabolism
  • Rats
  • Regeneration/drug effects
  • Respiratory Mucosa/drug effects
  • Signal Transduction/drug effects
  • Stem Cells/drug effects
  • TCF Transcription Factors/genetics
  • Time Factors
  • Transcription Factor 7-Like 2 Protein
  • Uteroglobin/genetics
  • beta Catenin/genetics


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