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A Battery of Motor Tests in a Neonatal Mouse Model of Cerebral Palsy
Published on: November 3, 2016
Cerebral Myelination in a Bronchopulmonary Dysplasia Murine Model
Wenwen Chen1,2,3, Ran Wang1,2, Chao Chen1,2
1Children's Hospital of Fudan University, Shanghai 201102, China.
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.
