Lung diseases like asthma and pulmonary hypertension could arise due to crosstalk between cells lining the lung (epithelial cells) and airway smooth muscle cells.
Already, it is known that such crosstalk is important in lung development.
Researchers at the University of Pennsylvania, Philadelphia, have now molecularly characterized one crosstalk pathway in mice, which could provide potential new therapeutic targets for treating individuals with lung diseases, such as asthma and pulmonary hypertension, which are caused, at least in part, by affects on airway smooth muscle cells.
The team, led by Edward Morrisey and Ethan David Cohen, used numerous in vivo gain- and loss-of-function approaches to demonstrate that a Wnt7b/Tnc/Pdgfr crosstalk pathway was important for mouse smooth muscle development.
They also showed that lung epithelial cells exclusively express Wnt7b and the developing airway smooth muscle cells express Pdgfr.
Particularly, expression of the components of this crosstalk pathway was upregulated in a mouse model of asthma and humans with pulmonary hypertension.
Thus indentifying the Wnt/Tnc/Pdgfr crosstalk pathway is equally important in both lung development and adult lung disease.