Ethanol Alters Cell Fate of Fetal Human Brain-Derived Stem and Progenitor Cells

摘要: Background:  Prenatal ethanol (ETOH) exposure can lead to fetal alcohol spectrum disorder (FASD). We previously showed that ETOH alters cell adhesion molecule gene expression and increases neurosphere size in brain-derived neural stem cells (NSC). Here, our aim was determine the effect of on fate NSC, premature glial-committed precursor (GCP), neuron-committed progenitor (NCP). Methods:  GCP, NCP were isolated from normal second-trimester human brains (n = 3) by positive selection using magnetic microbeads labeled with antibodies CD133 (NSC), A2B5 or PSA-NCAM (NCP). As a result small percentage each brain, NSC cultured mitogenic media for 72 hours produce neurospheres. The neurospheres primary isolates GCP used all experiments. Equal numbers 3 types treated either differentiating media, containing 0 100 mM ETOH, 120 hours. Expression Map2a, GFAP, O4 determined immunoflourescence microscopy western blot analysis. Fluorescence intensities quantified Metamorph software Molecular Devices, bands blots densitometry. Results:  promoted formation NCP. Under control conditions, attached differentiated, formed significantly smaller than those ETOH. Map2a increased reduced NCP, GFAP Gal-C presence compared controls. Conclusions:  This study shows neuronal cells. These alterations could contribute mechanism abnormal brain development FASD.