Reduction of Nfia gene expression and subsequent target genes by binge alcohol in the fetal brain
- Title
- Reduction of Nfia gene expression and subsequent target genes by binge alcohol in the fetal brain
- Author
- 정일엽
- Keywords
- Maternal alcohol consumption; Microarray analysis; FASD; Hippocampus
- Issue Date
- 2015-06
- Publisher
- ELSEVIER IRELAND LTD
- Citation
- NEUROSCIENCE LETTERS, v. 598, Page. 73-78
- Abstract
- The objective of the present study was to investigate the changes in gene expression in the fetal brain (forebrain and hippocampus) caused by maternal binge alcohol consumption. Pregnant C57BL/6J mice were treated intragastrically with distilled phosphate-buffered saline (PBS) or ethanol (2.9 g/kg) from embryonic day (ED) 8-12. Microarray analysis revealed that a significant number of genes were altered at ED 18 in the developing brain. Specifically, in hippocampus, nuclear factor one alpha (Nfia) and three N-methyl-D-aspartate (Nmda) receptors (Nmdar1, Nmdar2b, and Nmdar2d) were down-regulated. The transcription factor Nfia controls gliogenesis, cell proliferation and Nmda-induced neuronal survival by regulating the expression of target genes. Some of the Nfia-target gene (Aldh1a, Folh1, Gjb6, Fgf1, Neurod1, Sept4, and Ntsr2) expressions were also altered as expected. These results suggest that the altered expression of Nfia and Nmda receptors may be associated with the etiology of fetal alcohol syndrome (FAS). The data presented in this report will contribute to the understanding of the molecular mechanisms associated with the effects of alcohol in FASD individuals. (C) 2015 Elsevier Ireland Ltd. All rights reserved.
- URI
- http://www.sciencedirect.com/science/article/pii/S0304394015003651http://hdl.handle.net/20.500.11754/25200
- ISSN
- 0304-3940; 1872-7972
- DOI
- 10.1016/j.neulet.2015.05.016
- Appears in Collections:
- GRADUATE SCHOOL[S](대학원) > BIONANOTECHNOLOGY(바이오나노학과) > Articles
- Files in This Item:
There are no files associated with this item.
- Export
- RIS (EndNote)
- XLS (Excel)
- XML