Abstract：
:Airway smooth muscle is best known for its role as an airway constrictor in diseases such as asthma. However, its function in lung development is debated. A prevalent model, supported by in vitro data, posits that airway smooth muscle promotes lung branching through peristalsis and pushing intraluminal fluid to branching tips. Here, we test this model in vivo by inactivating Myocardin, which prevented airway smooth muscle differentiation. We found that Myocardin mutants show normal branching, despite the absence of peristalsis. In contrast, tracheal cartilage, vasculature, and neural innervation patterns were all disrupted. Furthermore, airway diameter is reduced in the mutant, counter to the expectation that the absence of smooth muscle constriction would lead to a more relaxed and thereby wider airway. These findings together demonstrate that during development, while airway smooth muscle is dispensable for epithelial branching, it is integral for building the tracheal architecture and promoting airway growth.
journal_name
Dev Celljournal_title
Developmental cellauthors
Young RE,Jones MK,Hines EA,Li R,Luo Y,Shi W,Verheyden JM,Sun Xdoi
10.1016/j.devcel.2020.02.001subject
Has Abstractpub_date
2020-04-06 00:00:00pages
73-85.e5issue
1eissn
1534-5807issn
1878-1551pii
S1534-5807(20)30070-8journal_volume
53pub_type
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