Associative DNA methylation changes in children with prenatal alcohol exposure

被引:66
作者
Laufer, Benjamin I. [1 ]
Kapalanga, Joachim [2 ]
Castellani, Christina A. [1 ]
Diehl, Eric J. [1 ]
Yan, Liying [3 ]
Singh, Shiva M. [1 ,2 ,4 ]
机构
[1] Univ Western Ontario, Dept Biol, Mol Genet Unit, London, ON N6A 5B7, Canada
[2] Univ Western Ontario, Dept Pediat, London, ON N6A 5B7, Canada
[3] EpigenDx Inc, Hopkinton, MA 01748 USA
[4] Univ Western Ontario, Program Neurosci, London, ON N6A 5B7, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
cohesin; CTCF; fetal alcohol spectrum disorders; glutamatergic synapse; hippo signaling; neurodevelopment; protocadherin; synapse; ETHANOL EXPOSURE; GAMMA-PROTOCADHERINS; GENE-EXPRESSION; MOUSE MODEL; SPECTRUM DISORDERS; BRAIN; DIVERSITY; CADHERINS; SURVIVAL; ALTERS;
D O I
10.2217/epi.15.60
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Aim: Prenatal alcohol exposure (PAE) can cause fetal alcohol spectrum disorders (FASD). Previously, we assessed PAE in brain tissue from mouse models, however whether these changes are present in humans remains unknown. Materials & methods: In this report, we show some identical changes in DNA methylation in the buccal swabs of six children with FASD using the 450K array. Results: The changes occur in genes related to protocadherins, glutamatergic synapses, and hippo signaling. The results were found to be similar in another heterogeneous replication group of six FASD children. Conclusion: The replicated results suggest that children born with FASD have unique DNA methylation defects that can be influenced by sex and medication exposure. Ultimately, with future clinical development, assessment of DNA methylation from buccal swabs can provide a novel strategy for the diagnosis of FASD.
引用
收藏
页码:1259 / 1274
页数:16
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