Establishment of smooth muscle and cartilage juxtaposition in the developing mouse upper airways

In the trachea and bronchi of the mouse, airway smooth muscle (SM) and cartilage are localized to complementary domains surrounding the airway epithelium. Proper juxtaposition of these tissues ensures a balance of elasticity and rigidity that is critical for effective air passage. It is unknown how...

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Bibliographic Details
Published in:Proceedings of the National Academy of Sciences - PNAS 2013-11, Vol.110 (48), p.19444-19449
Main Authors: Hines, Elizabeth A., Jones, Mary-Kayt N., Verheyden, Jamie M., Harvey, Julie F., Sun, Xin
Format: Article
Language:English
Subjects:
Animals
Biological Sciences
Bronchi
Bronchi - embryology
Cartilage
Cartilage - embryology
Cellular differentiation
Chondrocytes
Developmental biology
Epithelial cells
Epithelium
Fluorescent Antibody Technique
Gene expression
Genetics
Genotype & phenotype
In Situ Hybridization
Intestines
Lung - embryology
Lungs
Mesenchymal stem cells
Mice
Morphogenesis - physiology
Muscle, Smooth - embryology
Real-Time Polymerase Chain Reaction
Respiratory system
SOX9 Transcription Factor - metabolism
Tissues
Trachea
Trachea - embryology
Tracheomalacia - embryology
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Summary:In the trachea and bronchi of the mouse, airway smooth muscle (SM) and cartilage are localized to complementary domains surrounding the airway epithelium. Proper juxtaposition of these tissues ensures a balance of elasticity and rigidity that is critical for effective air passage. It is unknown how this tissue complementation is established during development. Here we dissect the developmental relationship between these tissues by genetically disrupting SM formation (through Srf inactivation) or cartilage formation (through Sox 9 inactivation) and assessing the impact on the remaining lineage. We found that, in the trachea and main bronchi, loss of SM or cartilage resulted in an increase in cell number of the remaining lineage, namely the cartilage or SM, respectively. However, only in the main bronchi, but not in the trachea, did the loss of SM or cartilage lead to a circumferential expansion of the remaining cartilage or SM domain, respectively. In addition to SM defects, cartilage-deficient tracheas displayed epithelial phenotypes, including decreased basal cell number, precocious club cell differentiation, and increased secretoglobin expression. These findings together delineate the mechanisms through which a cell-autonomous disruption of one structural tissue can have widespread consequences on upper airway function.
ISSN:0027-8424
1091-6490
DOI:10.1073/pnas.1313223110