Ethanol-induced transcriptional activation of programmed cell death 4 (Pdcd4) is mediated by GSK-3β signaling in rat cortical neuroblasts.

ABSTRACT: Ingestion of ethanol (ETOH) during pregnancy induces grave abnormalities in developing fetal brain. We have previously reported that ETOH induces programmed cell death 4 (PDCD4), a critical regulator of cell growth, in cultured fetal cerebral cortical neurons (PCNs) and in the cerebral cortex in vivo and affect protein synthesis as observed in Fetal Alcohol Spectrum Disorder (FASD). However, the mechanism which activates PDCD4 in neuronal systems is unclear and understanding this regulation may provide a counteractive strategy to correct the protein synthesis associated developmental changes seen in FASD. The present study investigates the molecular mechanism by which ethanol regulates PDCD4 in cortical neuroblasts, the immediate precursor of neurons. ETOH treatment significantly increased

SUBMITTER: Riar AK 

PROVIDER: S-EPMC4024002 | biostudies-literature | 2014

REPOSITORIES: biostudies-literature