Tenascin C is dysregulated in hypoplastic lungs of miR-200b−/− mice

Mouse model study reveals that absence of miR-200b causes dysregulation of Tenascin C protein in developing lungs, with decreased mesenchymal expression but increased airway localization. This imbalance in extracellular matrix protein distribution contributes to the lung hypoplasia phenotype seen in congenital diaphragmatic hernia.