作者: M.E. Charness , R.M. Safran , G. Perides
DOI: 10.1016/S0021-9258(17)37108-9
关键词: Morphogenesis 、 Biochemistry 、 Neural cell adhesion molecule 、 Cell biology 、 Adhesion 、 Cell adhesion 、 Cell growth 、 Cell 、 Cell–cell interaction 、 Cell adhesion molecule 、 Biology
摘要: Gestational exposure to ethanol causes defects in neuronal migration, fasciculation, and synaptogenesis, developmental events that depend on the patterned expression function of cell adhesion molecules (CAMs). Recombinant human osteogenic protein-1 (hOP-1) increases cell-cell promotes clustering proliferating neuroblastoma x glioma hybrid NG108-15 cells by strongly inducing N-CAM L1. Here we show concentrations achieved during social drinking inhibit hOP-1-induced without affecting proliferation, induction surface L1, or alternative splicing sialylation N-CAM. This inhibition was reproduced other alcohols proportion their chain length, but not teratogenic anticonvulsants phenylalanine. Ethanol hOP-1 morphogenesis inversely proportional concentration and, hence, levels Low (IC50 5-10 mM) inhibited hOP-1-treated cells, this action too more potently propanol butanol. may perturb brain skeletal development inhibiting CAM-mediated interactions.