Xinyan Wang1, Zhenshu Li1, Yun Zhu2,3, Jing Yan3,4, Huan Liu1,3, Guowei Huang1,3, Wen Li5,6. 1. Department of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin, 300070, China. 2. Department of Epidemiology and Biostatistics, School of Public Health, Tianjin Medical University, Tianjin, 300070, China. 3. Tianjin Key Laboratory of Environment, Nutrition and Public Health, Center for International Collaborative Research on Environment, Nutrition and Public Health, Tianjin, 300070, China. 4. Department of Social Medicine and Health Administration, School of Public Health, Tianjin Medical University, Tianjin, 300070, China. 5. Department of Nutrition and Food Science, School of Public Health, Tianjin Medical University, Tianjin, 300070, China. liwen828@tmu.edu.cn. 6. Tianjin Key Laboratory of Environment, Nutrition and Public Health, Center for International Collaborative Research on Environment, Nutrition and Public Health, Tianjin, 300070, China. liwen828@tmu.edu.cn.
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.
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.
Entities:
Keywords:
DNA methylation; Folic acid; Learning/memory; Pregnancy; Synaptic plasticity
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