ArticleEpigenetics & chromatin2019
Reduced H3K27me3 leads to abnormal Hox gene expression in neural tube defects.
Article in Epigenetics & chromatin, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 51 citations in OpenAlex.
- Associations of arsenic exposure and folate in maternal leukocyte DNA methylation: a case-control study of mothers with spina-bifida affected children.Environmental health : a global access science source · 2026Article
- Human organoids potentially boost research into environmental factors of neural tube defects.Reproductive toxicology (Elmsford, N.Y.) · 2025Review
- Molecular principles underlying aggressive cancers.Signal transduction and targeted therapy · 2025Review
- Genes related to neural tube defects and glioblastoma.Scientific reports · 2025Article
- Parental arsenic exposure and tissue-specific DNA methylation in Bangladeshi infants with spina bifida.Epigenetics · 2024Article
- Brain development and bioenergetic changes.Neurobiology of disease · 2024Review
- Up-regulation of miR-10a-5p expression inhibits the proliferation and differentiation of neural stem cells by targetingActa biochimica et biophysica Sinica · 2024Article
- Role of HOXA1-4 in the development of genetic and malignant diseases.Biomarker research · 2024Review
- Intergenerational association of gut microbiota and metabolism with perinatal folate metabolism and neural tube defects.iScience · 2023Article
- Changes inGenes · 2023Article
- A Semi-quantitative Evaluation of Out-to-Out Agenesis of Posterior Wall in a Dry Human Sacrum in Bangladesh.Cureus · 2022Article
- Epigenetic Changes and Chromatin Reorganization in Brain Function: Lessons from Fear Memory Ensemble and Alzheimer's Disease.International journal of molecular sciences · 2022Review
- Early anteroposterior regionalisation of human neural crest is shaped by a pro-mesodermal factor.eLife · 2022Article
- Sex-biased and parental allele-specific gene regulation by KDM6A.Biology of sex differences · 2022Article
- Folate-deficiency induced acyl-CoA synthetase short-chain family member 2 increases lysine crotonylome involved in neural tube defects.Frontiers in molecular neuroscience · 2022Article
- Abnormal transcriptome-wide DNA demethylation induced by folate deficiency causes neural tube defects.Frontiers in genetics · 2022Article
- Abnormal methylation caused by folic acid deficiency in neural tube defects.Open life sciences · 2022Review
- miR-222-3p is involved in neural tube closure by directly targeting Ddit4 in RA induced NTDs mouse model.Cell cycle (Georgetown, Tex.) · 2021Article
- Prenatal and postnatal traffic pollution exposure, DNA methylation in Shank3 and MeCP2 promoter regions, H3K4me3 and H3K27me3 and sociability in rats' offspring.Clinical epigenetics · 2021Article
- Knockdown screening of chromatin binding and regulatory proteins in zebrafish identified Suz12b as a regulator of tfpia and an antithrombotic drug target.Scientific reports · 2021Article
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundNeural tube defects (NTDs) are severe, common birth defects that result from failure of normal neural tube closure during early embryogenesis. Accumulating strong evidence indicates that genetic factors contribute to NTDs etiology, among them, HOX genes play a key role in neural tube closure. Although abnormal HOX gene expression can lead to NTDs, the underlying pathological mechanisms have not fully been understood.
methodWe detected that H3K27me3 and expression of the Hox genes in a retinoic acid (RA) induced mouse NTDs model on E8.5, E9.5 and E10.5 using RNA-sequencing and chromatin immunoprecipitation sequencing assays. Furthermore, we quantified 10 Hox genes using NanoString nCounter in brain tissue of fetuses with 39 NTDs patients including anencephaly, spina bifida, hydrocephaly and encephalocele.
resultsHere, our results showed differential expression in 26 genes with a > 20-fold change in the level of expression, including 10 upregulated Hox genes. RT-qPCR revealed that these 10 Hox genes were all upregulated in RA-induced mouse NTDs as well as RA-treated embryonic stem cells (ESCs). Using ChIP-seq assays, we demonstrate that a decrease in H3K27me3 level upregulates the expression of Hox cluster A-D in RA-induced mouse NTDs model on E10.5. Interestingly, RA treatment led to attenuation of H3K27me3 due to cooperate between UTX and Suz12, affecting Hox gene regulation. Further analysis, in human anencephaly cases, upregulation of 10 HOX genes was observed, along with aberrant levels of H3K27me3. Notably, HOXB4, HOXC4 and HOXD1 expression was negatively correlated with H3K27me3 levels.
conclusionOur results indicate that abnormal HOX gene expression induced by aberrant H3K27me3 levels may be a risk factor for NTDs and highlight the need for further analysis of genome-wide epigenetic modification in NTDs.
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