Glucocorticoids exacerbate hypoxia-induced expression of the pro-apoptotic gene Bnip3 in the developing cortex.

ABSTRACT: Neonatal administration of the synthetic glucocorticoid, dexamethasone (DEX) retards brain growth, alters adult behaviors and induces cell death in the rat brain, thereby implicating glucocorticoids as developmentally neuroendangering compounds. Glucocorticoids also increase expression of pro-apoptotic Bcl-2 family members and exacerbate expression of hypoxic responsive genes. Bnip3 is a pro-apoptotic Bcl-2 family member that is upregulated in response to hypoxia. In these studies, we investigated the interactions of glucocorticoid receptor and hypoxia in the regulation of Bnip3 mRNA in cortical neurons. Using quantitative real time reverse transcription-polymerase chain reaction, we found that DEX treatment of postnatal days 4-6 rat pups caused a significant increase in Bnip3 mRNA express

SUBMITTER: Sandau US 

PROVIDER: S-EPMC1832146 | biostudies-literature | 2007 Jan

REPOSITORIES: biostudies-literature