Research Article: Cerebral Myelination in a Bronchopulmonary Dysplasia Murine Model
Abstract:
Introduction: Bronchopulmonary dysplasia (BPD) is a devastating disease in preterm infants concurrent with neurodevelopmental disorders. Chronic hyperoxia exposure might also cause brain injury, but the evidence was insufficient. Methods: Neonatal C57BL/6J mice were exposed to hyperoxia from P0 to induce a BPD disease model. Lung histopathological morphology analyses were performed at P10, P15, and P20. Cerebral myelination was assessed using MBP (myelin basic protein, a major myelin protein), NfH (neurofilament heavy chain, a biomarker of neurofilament heavy chain), and GFAP (glial fibrillary acidic protein, a marker of astrocytes) as biomarkers by western blot and immunofluorescence. Results: Mice exposed to hyperoxia exhibited reduced and enlarged alveoli in lungs. During hyperoxia exposure, MBP declined at P10, but then increased to a comparable level to the air group at P15 and P20. Meanwhile, GFAP elevated significantly at P10, and the elevation sustained to P15 and P20. Conclusion: Neonatal hyperoxia exposure caused an arrest of lung development, as well as an obstacle of myelination process in white matter of the immature brain, with a decline of MBP in the generation period of myelin and persistent astrogliosis.
Introduction:
Neonatal hyperoxia exposure is frequent among preterm infants for lifesaving, particularly among those born with respiratory distress before 32 weeks of gestational age. For infants born preterm, even breathing the room’s normal air is hyperoxia relative to the fetus’ environment. Hyperoxia adds oxidative stress to the process of subsequent organ development after birth that might lead to developmental disturbances. Notably, hyperoxia is considered to be the key contributor to bronchopulmonary dysplasia (BPD). BPD…
Read more