Document Detail


beta-Catenin is not necessary for maintenance or repair of the bronchiolar epithelium.
MedLine Citation:
PMID:  19213872     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
Anna C Zemke; Roxana M Teisanu; Adam Giangreco; Jeff A Drake; Brian L Brockway; Susan D Reynolds; Barry R Stripp
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2009-02-12
Journal Detail:
Title:  American journal of respiratory cell and molecular biology     Volume:  41     ISSN:  1535-4989     ISO Abbreviation:  Am. J. Respir. Cell Mol. Biol.     Publication Date:  2009 Nov 
Date Detail:
Created Date:  2009-10-21     Completed Date:  2009-11-23     Revised Date:  2013-06-02    
Medline Journal Info:
Nlm Unique ID:  8917225     Medline TA:  Am J Respir Cell Mol Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  535-43     Citation Subset:  IM    
Affiliation:
Center for Lung Regeneration, Department of Environmental and Occupational Health, University of Pittsburgh, Pittsburgh, Pennsylvania, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Bronchioles / drug effects*,  metabolism,  pathology
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,  genetics
Respiratory Mucosa / drug effects*,  metabolism,  pathology
Signal Transduction* / drug effects,  genetics
Stem Cells / drug effects*,  metabolism,  pathology
TCF Transcription Factors / genetics
Time Factors
Transcription Factor 7-Like 2 Protein
Uteroglobin / genetics
beta Catenin / genetics,  metabolism*
Grant Support
ID/Acronym/Agency:
R01 HL064888/HL/NHLBI NIH HHS; R01 HL090146/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Catnb protein, mouse; 0/Naphthalenes; 0/RNA, Messenger; 0/Scgb1a1 protein, mouse; 0/TCF Transcription Factors; 0/Tcf7l2 protein, mouse; 0/Transcription Factor 7-Like 2 Protein; 0/beta Catenin; 2166IN72UN/naphthalene; 9060-09-7/Uteroglobin; EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases
Comments/Corrections

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