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Tenascin-C deficiency impairs alveolarization and microvascular maturation during postnatal lung development
Sonja I Mund1, Johannes C Schittny1
1Institute of Anatomy, University of Bern, Bern, Switzerland.
Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 21, 2020
Summary
Tenascin-C (TNC) deficiency delays lung alveolar septa formation and microvascular maturation in mice. However, a catch-up mechanism restores normal lung structure in adulthood, highlighting TNC's role in postnatal lung development.
Area of Science:
- Pulmonary biology and developmental biology
- Extracellular matrix protein function in organogenesis
Background:
- Lung gas exchange area increases post-birth via alveolarization and microvascular maturation.
- Tenascin-C (TNC), an extracellular matrix protein, is highly expressed during early postnatal lung development.
- TNC's role in prenatal lung development (branching morphogenesis) is previously established.
Purpose of the Study:
- To investigate the impact of Tenascin-C deficiency on postnatal lung alveolarization and microvascular maturation.
- To analyze cell proliferation and apoptosis during lung development in TNC-deficient mice.
Main Methods:
- Stereological analysis of alveolar septa formation and maturation in Tenascin-C deficient mice.
- Quantification of proliferating (Ki-67) and apoptotic (TUNEL) cells.
- Comparison of lung development at various postnatal time points (days 4-60) and adulthood.
Main Results:
- TNC deficiency caused delays in both classical and continued alveolarization phases.
- Increased cell proliferation at days 4-6 and increased TUNEL-positive cells at day 10 were observed.
- Premature microvascular maturation occurred at days 15-21, with less mature vasculature at day 60 in TNC-deficient mice; adult lungs showed no differences.
Conclusions:
- Tenascin-C is crucial for timely alveolar septa formation and microvascular maturation during postnatal lung development.
- TNC influences cell proliferation and migration essential for lung development.
- Despite developmental delays, compensatory mechanisms allow for normal adult lung structure in TNC-deficient mice.
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