Tenascin C is dysregulated in hypoplastic lungs of miR-200b−/− mice
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Read the article on link.springer.com ↗Article · Mar 2022 · 1 min read
In brief
In brief
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.
Written by the GCMD Library team from the article.
Abstract
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 × 107 ± 1 × 107; miR-200b−/−: 1.9 × 107 ± 5 × 106; 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.