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

Pediatr Surg Int

. 2022 Mar 2. doi: 10.1007/s00383-022-05096-0. Online ahead of print.

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

Moritz Markel 1 2Wai Hei Tse 1Nolan DeLeon 1Daywin Patel 1Shana Kahnamouizadeh 1Martin Lacher 2Richard Wagner 2Richard Keijzer 3Affiliations expand


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.

Keywords: Congenital diaphragmatic hernia; Pulmonary hypoplasia; Tenascin C; miR-200b.

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