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

Purpose We previously demonstrated that absence of miR-200b results in abnormal lung development in congenital diaphragmatic hernia due to imbalance between epithelial and mesenchymal cells. Tenascin C is a highly conserved extracellular matrix protein involved in epithelial to mesenchymal transition, tissue regeneration and lung development. Considering the involvement of Tenascin C and miR-200b and their potential interaction, we aimed to study Tenascin C during lung development in the absence of miR-200b. Methods We collected lungs of miR-200b −/− mice (male, 8 weeks). We performed Western blot (WB) analysis ( N = 6) and immunofluorescence ( N = 5) for Tenascin C and alpha smooth muscle actin and RT-qPCR for Tenascin C gene expression ( N = 4). Results Using WB analysis, we observed a decreased total protein abundance of Tenascin C in miR-200b −/− lungs (miR-200b +/+ : 3.8 × 10 7 ± 1 × 10 7 ; miR-200b −/− : 1.9 × 10 7 ± 5 × 10 6 ; p = 0.002). Immunofluorescence confirmed decreased total Tenascin C in miR-200b −/− lungs. Tenascin C was significantly decreased in the mesenchyme but relatively increased in the airways of mutant lungs. Total lung RNA expression of Tenascin C was higher in miR-200b −/− lungs. Conclusion We report dysregulation of Tenascin C in lungs of miR-200b −/− mice. This suggests that absence of miR-200b results in abnormal Tenascin C abundance contributing to the lung hypoplasia observed in miR-200b −/− mice.