Department of Neurosciences, University of New Mexico HSC, Albuquerque, NM, USA.
Department of Internal Medicine, University of New Mexico HSC, Albuquerque, NM, USA.
Alcohol Clin Exp Res. 2021 May;45(5):979-995. doi: 10.1111/acer.14590. Epub 2021 Apr 27.
Fetal alcohol syndrome (FAS) due to gestational alcohol exposure represents one of the most common causes of nonheritable lifelong disability worldwide. In vitro and in vivo models have successfully recapitulated multiple facets of the disorder, including morphological and behavioral deficits, but far less is understood regarding the molecular and genetic mechanisms underlying FAS.
In this study, we utilized an in vitro human pluripotent stem cell-based (hPSC) model of corticogenesis to probe the effects of early, chronic intermittent alcohol exposure on the transcriptome of first trimester-equivalent cortical neurons.
We used RNA sequencing of developing hPSC-derived neurons treated for 50 days with 50 mM ethanol and identified a relatively small number of biological pathways significantly altered by alcohol exposure. These included cell-type specification, axon guidance, synaptic function, and regional patterning, with a notable upregulation of WNT signaling-associated transcripts observed in alcohol-exposed cultures relative to alcohol-naïve controls. Importantly, this effect paralleled a shift in gene expression of transcripts associated with regional patterning, such that caudal forebrain-related transcripts were upregulated at the expense of more anterior ones. Results from H9 embryonic stem cells were largely replicated in an induced pluripotent stem cell line (IMR90-4), indicating that these patterning alterations are not cell line-specific.
We found that a major effect of chronic intermittent alcohol on the developing cerebral cortex is an overall imbalance in regionalization, with enrichment of gene expression related to the production of posterodorsal progenitors and a diminution of anteroventral progenitors. This finding parallels behavioral and morphological phenotypes observed in animal models of high-dose prenatal alcohol exposure, as well as patients with FAS.
由于妊娠期酒精暴露导致的胎儿酒精谱系障碍(FAS)是全球最常见的非遗传性终身残疾原因之一。体外和体内模型已成功重现了该疾病的多个方面,包括形态和行为缺陷,但对于导致 FAS 的分子和遗传机制,人们的了解还远远不够。
在这项研究中,我们利用体外人类多能干细胞(hPSC)皮质发生模型,探究早期慢性间歇性酒精暴露对相当于妊娠早期皮质神经元转录组的影响。
我们对用 50mM 乙醇处理 50 天的发育中的 hPSC 衍生神经元进行 RNA 测序,发现有相当数量的生物学途径被酒精暴露显著改变。这些途径包括细胞类型特化、轴突导向、突触功能和区域模式形成,与酒精未处理对照相比,酒精暴露培养物中观察到 WNT 信号相关转录物的显著上调。重要的是,这种效应与与区域模式形成相关的转录物的基因表达变化相平行,使得后脑相关转录物上调,而更靠前的转录物下调。胚胎干细胞 H9 的结果在诱导多能干细胞系(IMR90-4)中得到了很大程度的复制,表明这些模式改变不是细胞系特异性的。
我们发现慢性间歇性酒精对发育中的大脑皮层的主要影响是整体区域化失衡,与产生后背侧祖细胞相关的基因表达富集,而与前腹侧祖细胞相关的基因表达减少。这一发现与高剂量产前酒精暴露动物模型以及 FAS 患者观察到的行为和形态表型相平行。