التفاصيل البيبلوغرافية
| العنوان: |
Tenascin C is dysregulated in hypoplastic lungs of miR-200b−/− mice. |
| المؤلفون: |
Markel, Moritz, Tse, Wai Hei, DeLeon, Nolan, Patel, Daywin, Kahnamouizadeh, Shana, Lacher, Martin, Wagner, Richard, Keijzer, Richard |
| المصدر: |
Pediatric Surgery International; May2022, Vol. 38 Issue 5, p695-700, 6p |
| مصطلحات موضوعية: |
TENASCIN, EXTRACELLULAR matrix proteins, EPITHELIAL-mesenchymal transition, LUNGS, DIAPHRAGMATIC hernia |
| مستخلص: |
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. [ABSTRACT FROM AUTHOR] |
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| قاعدة البيانات: |
Complementary Index |
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