ArticleNutrients2021
Prenatal Iron Deficiency and Choline Supplementation Interact to Epigenetically Regulate
Article in Nutrients, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Dysfunctional connectivity within hippocampal and entorhinal networks underlies early-life iron deficiency induced social recognition deficits, a preliminary study.Scientific reports · 2026Article
- Article
- Emerging Epigenetic Therapeutics and Diagnostics for Autism Spectrum Disorder.Current issues in molecular biology · 2025Review
- Effects of prenatal iron deficiency on neurological development and related disorders in offspring.Frontiers in nutrition · 2025Review
- Zhi-zi-chi decoction mitigates depression by enhancing lncRNA Six3os1 expression and promoting histone H3K4 methylation at the BDNF promoter.Journal of cellular and molecular medicine · 2024Article
- Identification of Genes Responding to Iron or Choline Treatment for Early-Life Iron Deficiency in the Male Rat Hippocampal Transcriptomes.The Journal of nutrition · 2024Article
- Chromatin accessibility and H3K9me3 landscapes reveal long-term epigenetic effects of fetal-neonatal iron deficiency in rat hippocampus.BMC genomics · 2024Article
- Review
- Gestational iron deficiency affects the ratio between interneuron subtypes in the postnatal cerebral cortex in mice.Development (Cambridge, England) · 2023Article
- Sex-Specific Effects of Early-Life Iron Deficiency and Prenatal Choline Treatment on Adult Rat Hippocampal Transcriptome.Nutrients · 2023Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Early-life iron deficiency (ID) causes long-term neurocognitive impairments and gene dysregulation that can be partially mitigated by prenatal choline supplementation. The long-term gene dysregulation is hypothesized to underlie cognitive dysfunction. However, mechanisms by which iron and choline mediate long-term gene dysregulation remain unknown. In the present study, using a well-established rat model of fetal-neonatal ID, we demonstrated that ID downregulated hippocampal expression of the gene encoding JmjC-ARID domain-containing protein 1B (JARID1B), an iron-dependent histone H3K4 demethylase, associated with a higher histone deacetylase 1 (HDAC1) enrichment and a lower enrichment of acetylated histone H3K9 (H3K9ac) and phosphorylated cAMP response element-binding protein (pCREB). Likewise, ID reduced transcriptional capacity of the gene encoding brain-derived neurotrophic factor (BDNF), a target of JARID1B, associated with repressive histone modifications such as lower H3K9ac and pCREB enrichments at the
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