Neonatal Periostin Knockout Mice Are Protected from Hyperoxia-Induced Alveolar Simplication

摘要: In bronchopulmonary dysplasia (BPD), alveolar septae are thickened with collagen and α-smooth muscle actin, transforming growth factor (TGF)-β-positive myofibroblasts. Periostin, a secreted extracellular matrix protein, is involved in TGF-β-mediated fibrosis myofibroblast differentiation. We hypothesized that periostin expression required for hypoalveolarization interstitial hyperoxia-exposed neonatal mice, an animal model this disease. also examined lung mesenchymal stromal cells tissue of mice human infants BPD. Two-to-three day-old wild-type null were exposed to air or 75% oxygen 14 days. Mesenchymal isolated from tracheal aspirates premature infants. Hyperoxic exposure increased wall expression, particularly areas thickening. Periostin co-localized suggesting synthesis by A similar pattern was found sections dying Unlike did not show larger spaces muscle-positive Compared showed reduced mRNA elastin, CXCL1, CXCL2 CCL4. TGF-β treatment cell DNA conclude the lungs BPD, hyperoxia-induced fibrosis.