Tyler Christina R, Allan Andrea M
Department of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Department of Neurosciences, University of New Mexico Health Sciences Center, Albuquerque, NM 87131, USA.
Alcohol. 2014 Aug;48(5):483-92. doi: 10.1016/j.alcohol.2014.06.001. Epub 2014 Jun 7.
Prenatal alcohol exposure can lead to long-lasting changes in functional and genetic programs of the brain, which may underlie behavioral alterations seen in Fetal Alcohol Spectrum Disorder (FASD). Aberrant fetal programming during gestational alcohol exposure is a possible mechanism by which alcohol imparts teratogenic effects on the brain; however, current methods used to investigate the effects of alcohol on development often rely on either direct application of alcohol in vitro or acute high doses in vivo. In this study, we used our established moderate prenatal alcohol exposure (PAE) model, resulting in maternal blood alcohol content of approximately 20 mM, and subsequent ex vivo cell culture to assess expression of genes related to neurogenesis. Proliferating and differentiating neural progenitor cell culture conditions were established from telencephalic tissue derived from embryonic day (E) 15-17 tissue exposed to alcohol via maternal drinking throughout pregnancy. Gene expression analysis on mRNA derived in vitro was performed using a microarray, and quantitative PCR was conducted for genes to validate the microarray. Student's t tests were performed for statistical comparison of each exposure under each culture condition using a 95% confidence interval. Eleven percent of genes on the array had significantly altered mRNA expression in the prenatal alcohol-exposed neural progenitor culture under proliferating conditions. These include reduced expression of Adora2a, Cxcl1, Dlg4, Hes1, Nptx1, and Vegfa and increased expression of Fgf13, Ndn, and Sox3; bioinformatics analysis indicated that these genes are involved in cell growth and proliferation. Decreased levels of Dnmt1 and Dnmt3a were also found under proliferating conditions. Under differentiating conditions, 7.3% of genes had decreased mRNA expression; these include Cdk5rap3, Gdnf, Hey2, Heyl, Pard6b, and Ptn, which are associated with survival and differentiation as indicated by bioinformatics analysis. This study is the first to use chronic low to moderate PAE, to more accurately reflect maternal alcohol consumption, and subsequent neural progenitor cell culture to demonstrate that PAE throughout gestation alters expression of genes involved in neural development and embryonic neurogenesis.
孕期酒精暴露可导致大脑功能和基因程序发生长期变化,这可能是胎儿酒精谱系障碍(FASD)中所见行为改变的基础。孕期酒精暴露期间异常的胎儿编程是酒精对大脑产生致畸作用的一种可能机制;然而,目前用于研究酒精对发育影响的方法通常要么依赖于在体外直接应用酒精,要么依赖于在体内给予急性高剂量酒精。在本研究中,我们使用已建立的中度孕期酒精暴露(PAE)模型,使母体血液酒精含量约为20 mM,随后进行体外细胞培养以评估与神经发生相关的基因表达。从妊娠期间通过母体饮酒暴露于酒精的胚胎第15 - 17天的端脑组织建立增殖和分化神经祖细胞培养条件。使用微阵列对体外衍生的mRNA进行基因表达分析,并对基因进行定量PCR以验证微阵列。使用95%置信区间进行学生t检验,以对每种培养条件下的每种暴露进行统计比较。在增殖条件下,阵列上11%的基因在产前酒精暴露的神经祖细胞培养物中的mRNA表达有显著改变。这些包括Adora2a、Cxcl1、Dlg4、Hes1、Nptx1和Vegfa的表达降低,以及Fgf13、Ndn和Sox3的表达增加;生物信息学分析表明这些基因参与细胞生长和增殖。在增殖条件下还发现Dnmt1和Dnmt3a水平降低。在分化条件下,7.3%的基因mRNA表达降低;这些包括Cdk5rap3、Gdnf、Hey2、Heyl、Pard6b和Ptn,生物信息学分析表明它们与存活和分化相关。本研究首次使用慢性低至中度PAE,以更准确地反映母体酒精摄入量,随后进行神经祖细胞培养,以证明整个妊娠期的PAE会改变参与神经发育和胚胎神经发生的基因表达。