ArticleChildren (Basel, Switzerland)2023
Cerebral Myelination in a Bronchopulmonary Dysplasia Murine Model.
Article in Children (Basel, Switzerland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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2 citing papers in PubMed, 2 citations in OpenAlex.
- Developmentally sensitive neuropharmacological effects of dexamethasone in neonatal bronchopulmonary dysplasia-associated brain injury via microglial Acod1-itaconate/IL-1β signaling.Frontiers in pharmacology · 2026Article
- A rat model establishment of bronchopulmonary dysplasia-related lung & brain injury within 28 days after birth.BMC neuroscience · 2024Article
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3 authors at 1 institution in 1 country.
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Abstract
introductionBronchopulmonary 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.
methodsNeonatal 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.
resultsMice 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.
conclusionNeonatal 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.
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