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母体叶酸会影响雄性大鼠后代的DNA甲基化谱,这与神经发育和学习/记忆能力有关。

Maternal folic acid impacts DNA methylation profile in male rat offspring implicated in neurodevelopment and learning/memory abilities.

作者信息

Wang Xinyan, Li Zhenshu, Zhu Yun, Yan Jing, Liu Huan, Huang Guowei, Li Wen

机构信息

Department of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin, 300070, China.

Department of Epidemiology and Biostatistics, School of Public Health, Tianjin Medical University, Tianjin, 300070, China.

出版信息

Genes Nutr. 2021 Jan 11;16(1):1. doi: 10.1186/s12263-020-00681-1.

DOI:10.1186/s12263-020-00681-1
PMID:33430764
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7802276/
Abstract

BACKGROUND

Periconceptional folic acid (FA) supplementation not only reduces the incidence of neural tube defects, but also improves cognitive performances in offspring. However, the genes or pathways that are epigenetically regulated by FA in neurodevelopment were rarely reported.

METHODS

To elucidate the underlying mechanism, the effect of FA on the methylation profiles in brain tissue of male rat offspring was assessed by methylated DNA immunoprecipitation chip. Differentially methylated genes (DMGs) and gene network analysis were identified using DAVID and KEGG pathway analysis.

RESULTS

Compared with the folate-normal diet group, 1939 DMGs were identified in the folate-deficient diet group, and 1498 DMGs were identified in the folate-supplemented diet group, among which 298 DMGs were overlapped. The pathways associated with neurodevelopment and learning/memory abilities were differentially methylated in response to maternal FA intake during pregnancy, and there were some identical and distinctive potential mechanisms under FA deficiency or FA-supplemented conditions.

CONCLUSIONS

In conclusion, genes and pathways associated with neurodevelopment and learning/memory abilities were differentially methylated in male rat offspring in response to maternal FA deficiency or supplementation during pregnancy.

摘要

背景

孕期补充叶酸不仅能降低神经管缺陷的发生率,还能改善后代的认知能力。然而,叶酸在神经发育过程中通过表观遗传调控的基因或信号通路鲜有报道。

方法

为阐明潜在机制,采用甲基化DNA免疫沉淀芯片评估叶酸对雄性大鼠后代脑组织甲基化图谱的影响。使用DAVID和KEGG通路分析鉴定差异甲基化基因(DMG)和基因网络。

结果

与叶酸正常饮食组相比,叶酸缺乏饮食组鉴定出1939个DMG,叶酸补充饮食组鉴定出1498个DMG,其中298个DMG重叠。孕期母体叶酸摄入会使与神经发育和学习/记忆能力相关的信号通路发生差异甲基化,在叶酸缺乏或补充叶酸的条件下存在一些相同和独特的潜在机制。

结论

总之,孕期母体叶酸缺乏或补充叶酸会使雄性大鼠后代中与神经发育和学习/记忆能力相关的基因和信号通路发生差异甲基化。

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