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

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

doi:10.1186/s12263-020-00681-1

Cited by 22 publications

(10 citation statements)

References 56 publications

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“…[ 25–29 ] Recently, many researchers pointed that prenatal malnutrition was closely linked with development of multiple organs via different mechanisms in offspring. [ 30–33 ] In the present study, we first validated that prenatal high‐sucrose diet increased maternal weight before delivery, but it had no effect on the fetal number. Consistent with a population‐based cohort study with 40 years of follow‐up investigated that prenatal hyperglycemia increased rates of early onset cardiovascular diseases from childhood to early adulthood, [ 34 ] our previous data confirmed that prenatal high sucrose impaired the micro‐vascular function of adult and aged offspring.…”

Section: Discussionsupporting

confidence: 51%

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring

Feng

Zhang

et al. 2021

Molecular Nutrition Food Res

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Scope Maternal nutrition during pregnancy is related to intrauterine fetal development. The authors’ previous work reports that prenatal high sucrose (HS) diet impaired micro‐vascular functions in postnatal offspring. It is unclear whether/how prenatal HS causes vascular injury during fetal life. Methods and results Pregnant rats are fed with normal drinking water or 20% high‐sucrose solution during the whole gestational period. Pregnant HS increases maternal weight before delivery. Fetal thoracic aorta is separated for experiments. Angiotensin II (AII)‐stimulated vascular contraction of fetal thoracic arteries in HS group is greater, which mainly results from the enhanced AT1 receptor (AT1R) function and the downstream signaling. Nifedipine significantly increases vascular tension in HS group, indicating that the L‐type calcium channels (LTCCs) function is strengthened. 2‐Aminoethyl diphenylborinate (2‐APB), inositol 1,4,5‐trisphosphate receptors (IP3Rs) inhibitor, increases vascular tension induced by AII in HS group and ryanodine receptors‐sensitive vascular tone shows no difference in the two groups, which suggested that the activity of IP3Rs‐operated calcium channels is increased. Conclusion These findings suggest that prenatal HS induces vascular dysfunction of thoracic arteries in fetal offspring by enhancing AT1R, LTCCs function and IP3Rs‐associated calcium channels, providing new information regarding the impact of prenatal HS on the functional development of fetal vascular systems.

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Section: Discussionsupporting

confidence: 51%

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring

Feng

Zhang

et al. 2021

Molecular Nutrition Food Res

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“…Based on the above analysis, it can be concluded that HAR1A take an important role in neuroactive ligand-receptor, synaptic and axon guidance. Those are all critical processes in the early development of the brain (33). Neurons migrate to proper locations to make connections by emitting axons during the development of the brain (34).…”

Section: Discussionmentioning

confidence: 99%

Identify the regulatory network of LncRNA HAR1A in neurological development by RNA-Sequencing and bioinformatics analysis.

Zhang

Lin

et al. 2022

Preprint

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Background: LncRNA HAR1A, which is explicitly expressed in Cajal-Retzius neurons (CRs), has been reported to be related to the development of the human brain. As one of the human accelerated regions (HARs) gene, it plays an important role in central neural evolution. Dysregulation of lncRNA HAR1A was associated with many central nervous system diseases. Methods:We cloned human gene HAR1A into the EF-1α promoter vector to make the transgenic mice. To observe the changes in memory and cognitive ability of mice, we conducted the Morris water maze (MWM) test and step-down passive avoidance test. RNA-seq analysis was performed to identify the differentially expressed genes (DEGs) of the experiment and control group. Systematic bioinformatic analysis was used to confirm the pathway and function that the DEGs enriched in. 523 human gene expression datasets were downloaded from The Cancer Genome Atlas (TCGA) for Co-expression analysis. Through Co-expression analysis, we obtained the Protein-Protein Interactions Network (PPI-Net) and enrichment pathways of LncRNA HAR1A's co-expression genes in human. Results:The memory and cognitive ability of the transgene mice were significantly improved. Results of GO analysis showed that cerebral cortex development is the most significant function related to HAR1A in brain development. DEGs enriched in this function included Lhx2, Emx2, Foxg1, Nr2e1, Emx1. They all play an important role in the regulation of CRs' function. "Cellular response to calcium ion" exhibited the highest rich factor in the Gene Ontology (GO) analysis. Core genes in the PPI-Net were SNAP25, GRIN1, SYN1, DLG4, CAMK2A. SNAP25, SYN1 relate to synaptic function. GRIN1, DLG4 and CAMK2A relate to synapse formation. GO and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis of DEGs and HAR1A 's Co-expressed genes in 523 human gene expression datasets show that synapse, axon guidance, synaptic signaling and ligand-receptor interaction are significant.Conclusions:Overexpress HAR1A will improve the memory and cognitive ability of the transgene mice. The possible mechanism is HAR1A affects brain development by regulating CRs' function. Moreover, HAR1A may be involved in ligand-receptor interaction, Axon guidance and synapse formation, which are important for brain development and evolution. Cellular response to calcium may play an important role in those process.

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“…It is known from animal studies that folic acid supplementation impacts DNA methylation implicated in neurodevelopment and learning/memory abilities [77]. In this review, evidence of the benefit of folic acid supplement use, and the timing at which supplementation was initiated, on foetal brain development was inconsistent.…”

Section: Folic Acid Supplement Usementioning

confidence: 99%

Maternal One-Carbon Metabolism during the Periconceptional Period and Human Foetal Brain Growth: A Systematic Review

Rubini

Baijens

Horánszky

et al. 2021

Genes

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The maternal environment during the periconceptional period influences foetal growth and development, in part, via epigenetic mechanisms moderated by one-carbon metabolic pathways. During embryonic development, one-carbon metabolism is involved in brain development and neural programming. Derangements in one-carbon metabolism increase (i) the short-term risk of embryonic neural tube-related defects and (ii) long-term childhood behaviour, cognition, and autism spectrum disorders. Here we investigate the association between maternal one-carbon metabolism and foetal and neonatal brain growth and development. Database searching resulted in 26 articles eligible for inclusion. Maternal vitamin B6, vitamin B12, homocysteine, and choline were not associated with foetal and/or neonatal head growth. First-trimester maternal plasma folate within the normal range (> 17 nmol/L) associated with increased foetal head size and head growth, and high erythrocyte folate (1538–1813 nmol/L) with increased cerebellar growth, whereas folate deficiency (< 7 nmol/L) associated with a reduced foetal brain volume. Preconceptional folic acid supplement use and specific dietary patterns (associated with increased B vitamins and low homocysteine) increased foetal head size. Although early pregnancy maternal folate appears to be the most independent predictor of foetal brain growth, there is insufficient data to confirm the link between maternal folate and offspring risks for neurodevelopmental diseases.

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

Cited by 22 publications

References 56 publications

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring

Prenatal High‐Sucrose Diet Induced Vascular Dysfunction in Thoracic Artery of Fetal Offspring

Identify the regulatory network of LncRNA HAR1A in neurological development by RNA-Sequencing and bioinformatics analysis.

Maternal One-Carbon Metabolism during the Periconceptional Period and Human Foetal Brain Growth: A Systematic Review

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