Project description:Declining lung function in patients with interstitial lung disease is accompanied by epithelial remodeling and progressive scarring of the gas-exchange region. There is a need to better understand the contribution of basal cell hyperplasia and associated mucosecretory dysfunction to the development of idiopathic pulmonary fibrosis (IPF).We confirmed that Notch2 maintains undifferentiated basal cells and restrict basal-to-ciliated differentiation, and present evidence that Notch3 functions to restrain secretory differentiation. When characterizing single cell transcriptomes of the IPF lung we found a bias towards accumulation of the secretory primed basal cell subset.
