This idea is supported by observations made in the mouse hyperoxia BPD model, where increased expression of Itgav, encoding the αv integrin subunit [which also binds fibronectin; (67)], was noted (51), and was accompanied by impaired alveolarization and increased Fbln5 expression and TGF-β activity, and aberrant elastin fiber deposition. This evidence concerns the gene TGFB1 and bronchopulmonary dysplasia.