Postnatal glucocorticoids suppress myelination in a dose-dependent manner by genomic mechanism

ABSTRACT: Objective: Postnatal glucocorticoids (GCs) are widely used in the prevention of chronic lung disease in premature infants. However, their use is associated with neurodevelopmental delay and cerebral palsy. We hypothesized that postnatal dexamethasone or betamethasone in high-dose, but not low-dose, would induce hypomyelination, astrogliosis, and motor impairment in premature rabbit pups. Additionally, these effects would be mediated by glucocorticoid receptors (GRs). Methods: Preterm rabbit pups, delivered by C-section at E29 (term=32d), were treated with a high dose of dexamethasone or vehicle. Myelin basic protein (MBP), glial fibrillary basic protein (GFAP), oligodendrocyte proliferation and maturation, and alteration of transcriptomic profile were evaluated in these pups. Neurobehavi

ORGANISM(S): Oryctolagus cuniculus

SUBMITTER: Dumitru Iacobas 

PROVIDER: E-GEOD-44610 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress