Key result
Continuous 85% oxygen exposure prematurely downregulated Periostin and αSMA expression before distal lung simplification, identifying Periostin as an early biomarker of inhibited alveolar septation.
Why the study?
Does continuous hyperoxia alter Postn expression and alveolarization in neonatal mice?
Population
Neonatal C57BL/6J mice and Postn knockout mice
Comparison
Continuous hyperoxia (85%-O₂ or 60%-O₂) vs Room-air (21%-O₂)
Design
Preclinical
Follow-up
14 days (from birth P0 to P14)
Authors
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Periostin may mark early hyperoxia lung injury in neonates; leaves open translation to preterm bronchopulmonary dysplasia.
Does continuous hyperoxia alter Postn expression and alveolarization in neonatal mice?
Periostin downregulation is an early biomarker of acutely inhibited alveolar septation in hyperoxia-induced lung injury in neonatal mice.
Ahlfeld et al. (2013) studied Hyperoxic lung injury. Continuous hyperoxia vs. Room-air (21%-O₂) was evaluated on Postn and αSMA expression and alveolarization. Continuous 85% oxygen exposure prematurely downregulated Periostin and αSMA expression before distal lung simplification, identifying Periostin as an early biomarker of inhibited alveolar septation.
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