ArticlePloS one2015
Multiple Antenatal Dexamethasone Treatment Alters Brain Vessel Differentiation in Newborn Mouse Pups.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Stress in utero: prenatal dexamethasone exposure causes greater structural gliovascular alterations in female offspring than in males.Frontiers in neuroscience · 2025Article
- Prednisolone Targets Claudins in Mouse Brain Blood Vessels.International journal of molecular sciences · 2023Article
- Maternal Undernutrition Modulates Neonatal Rat Cerebrovascular Structure, Function, and Vulnerability to Mild Hypoxic-Ischemic Injury via Corticosteroid-Dependent and -Independent Mechanisms.International journal of molecular sciences · 2021Article
- Plasminogen activator inhibitor-1 augments damage by impairing fibrinolysis after traumatic brain injury.Annals of neurology · 2019Article
- Death or resolution: the "natural history" of pulmonary hypertension in bronchopulmonary dysplasia.Journal of perinatology : official journal of the California Perinatal Association · 2019Article
- Efficacy and safety of antenatal steroids.American journal of physiology. Regulatory, integrative and comparative physiology · 2018Review
- Brain endothelial cell junctions after cerebral hemorrhage: Changes, mechanisms and therapeutic targets.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018Review
- Barriers to Drug Distribution into the Perinatal and Postnatal Brain.Pharmaceutical research · 2018Review
- Clobetasol promotes remyelination in a mouse model of neuromyelitis optica.Acta neuropathologica communications · 2016Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antenatal steroid treatment decreases morbidity and mortality in premature infants through the maturation of lung tissue, which enables sufficient breathing performance. However, clinical and animal studies have shown that repeated doses of glucocorticoids such as dexamethasone and betamethasone lead to long-term adverse effects on brain development. Therefore, we established a mouse model for antenatal dexamethasone treatment to investigate the effects of dexamethasone on brain vessel differentiation towards the blood-brain barrier (BBB) phenotype, focusing on molecular marker analysis. The major findings were that in total brains on postnatal day (PN) 4 triple antenatal dexamethasone treatment significantly downregulated the tight junction protein claudin-5, the endothelial marker Pecam-1/CD31, the glucocorticoid receptor, the NR1 subunit of the N-methyl-D-aspartate receptor, and Abc transporters (Abcb1a, Abcg2 Abcc4). Less pronounced effects were found after single antenatal dexamethasone treatment and in PN10 samples. Comparisons of total brain samples with isolated brain endothelial cells together with the stainings for Pecam-1/CD31 and claudin-5 led to the assumption that the morphology of brain vessels is affected by antenatal dexamethasone treatment at PN4. On the mRNA level markers for angiogenesis, the sonic hedgehog and the Wnt pathway were downregulated in PN4 samples, suggesting fundamental changes in brain vascularization and/or differentiation. In conclusion, we provided a first comprehensive molecular basis for the adverse effects of multiple antenatal dexamethasone treatment on brain vessel differentiation.
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