ArticleScientific reports2017
Overexpression of DNMT3b target genes during Enteric Nervous System development contribute to the onset of Hirschsprung disease.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 23 citations in OpenAlex.
- Hirschsprung's disease: m6A methylase VIRMA suppresses cell migration and proliferation by regulating GSK3β.Pediatric research · 2024Article
- The roles of non-coding RNAs in Hirschsprung's disease.Non-coding RNA research · 2024Review
- BAP1 is required prenatally for differentiation and maintenance of postnatal murine enteric nervous system.The Journal of clinical investigation · 2024Article
- Review
- Genome-wide analysis of DNA methylation in Hirschsprung enteric precursor cells: unraveling the epigenetic landscape of enteric nervous system development.Clinical epigenetics · 2021Article
- Development, Diversity, and Neurogenic Capacity of Enteric Glia.Frontiers in cell and developmental biology · 2021Review
- ChIP-Seq-Based Approach in Mouse Enteric Precursor Cells Reveals New Potential Genes with a Role in Enteric Nervous System Development and Hirschsprung Disease.International journal of molecular sciences · 2020Article
- Association betweenThe Journal of international medical research · 2020Article
- Identification of New Potential LncRNA Biomarkers in Hirschsprung Disease.International journal of molecular sciences · 2020Article
- "Too much guts and not enough brains": (epi)genetic mechanisms and future therapies of Hirschsprung disease - a review.Clinical epigenetics · 2019Review
- Epigenetic Mechanisms in Hirschsprung Disease.International journal of molecular sciences · 2019Review
- Down-regulation of circ-PRKCI inhibits cell migration and proliferation in Hirschsprung disease by suppressing the expression of miR-1324 target PLCB1.Cell cycle (Georgetown, Tex.) · 2018Article
- DNMT3B Functions: Novel Insights From Human Disease.Frontiers in cell and developmental biology · 2018Review
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Authors and funding
7 authors at 3 institutions in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Hirschsprung disease (HSCR) is attributed to a failure of neural crest cells (NCCs) to migrate, proliferate, differentiate and/or survive in the bowel wall during embryonic Enteric Nervous System (ENS) development. ENS formation is the result from a specific gene expression pattern regulated by epigenetic events, such DNA methylation by the DNA methyltransferases (DNMTs), among other mechanisms. Specifically, DNMT3b de novo methyltransferase is associated with NCCs development and has been shown to be implicated in ENS formation and in HSCR. Aiming to elucidate the specific mechanism underlying the DNMT3b role in such processes, we have performed a chromatin immunoprecipitation coupled with massively parallel sequencing analysis to identify the DNMT3B target genes in enteric precursor cells (EPCs) from mice. Moreover, the expression patterns of those target genes have been analyzed in human EPCs from HSCR patients in comparison with controls. Additionally, we have carried out a search of rare variants in those genes in a HSCR series. Through this approach we found 9 genes showing a significantly different expression level in both groups. Therefore, those genes may have a role in the proper human ENS formation and a failure in their expression pattern might contribute to this pathology.
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