Evidence map›Paper›PMID 23776576›Full record

ArticlePloS one2013

Analysis of epigenetic factors in mouse embryonic neural stem cells exposed to hyperglycemia.

Sukanya Shyamasundar, Shweta P Jadhav, Boon Huat Bay, Samuel Sam Wah Tay, S Dinesh Kumar, Danny Rangasamy, S Thameem Dheen

Abstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed.

  1. Article
  2. Review
  3. Article
  4. Article
  5. Review
  6. Role of Diet in Stem and Cancer Stem Cells.International journal of molecular sciences · 2022
    Review
  7. Cerebral Effects of Neonatal Dysglycemia.Clinics in perinatology · 2022
    Review
  8. Article
  9. Review
  10. Article
  11. Review
  12. Article
  13. Article
  14. Sensory Neuropathy Affects Cardiac miRNA Expression Network TargetingInternational journal of molecular sciences · 2019
    Article
  15. Review
  16. Article
  17. Arsenic Induces Members of the mmu-miR-466-669 Cluster Which Reduces NeuroD1 Expression.Toxicological sciences : an official journal of the Society of Toxicology · 2018
    Article
  18. Review
  19. Article
  20. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors.

Sukanya ShyamasundarDepartment of Anatomy, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, Singapore.
Shweta P Jadhav
Boon Huat Bay
Samuel Sam Wah Tay
S Dinesh Kumar
Danny Rangasamy
S Thameem Dheen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMaternal diabetes alters gene expression leading to neural tube defects (NTDs) in the developing brain. The mechanistic pathways that deregulate the gene expression remain unknown. It is hypothesized that exposure of neural stem cells (NSCs) to high glucose/hyperglycemia results in activation of epigenetic mechanisms which alter gene expression and cell fate during brain development. METHODS AND

findingsNSCs were isolated from normal pregnancy and streptozotocin induced-diabetic pregnancy and cultured in physiological glucose. In order to examine hyperglycemia induced epigenetic changes in NSCs, chromatin reorganization, global histone status at lysine 9 residue of histone H3 (acetylation and trimethylation) and global DNA methylation were examined and found to be altered by hyperglycemia. In NSCs, hyperglycemia increased the expression of Dcx (Doublecortin) and Pafah1b1 (Platelet activating factor acetyl hydrolase, isoform 1b, subunit 1) proteins concomitant with decreased expression of four microRNAs (mmu-miR-200a, mmu-miR-200b, mmu-miR-466a-3p and mmu-miR-466 d-3p) predicted to target these genes. Knockdown of specific microRNAs in NSCs resulted in increased expression of Dcx and Pafah1b1 proteins confirming target prediction and altered NSC fate by increasing the expression of neuronal and glial lineage markers. CONCLUSION/

interpretationThis study revealed that hyperglycemia alters the epigenetic mechanisms in NSCs, resulting in altered expression of some development control genes which may form the basis for the NTDs. Since epigenetic changes are reversible, they may be valuable therapeutic targets in order to improve fetal outcomes in diabetic pregnancy.

Indexed as

1-Alkyl-2-acetylglycerophosphocholine EsteraseAnimalsCells, CulturedDNA MethylationDoublecortin Domain ProteinsDoublecortin ProteinEmbryo, MammalianEmbryonic Stem CellsEpigenesis, GeneticFemaleGlucoseHistonesHyperglycemiaMiceMicroRNAsMicrotubule-Associated Proteins1-Alkyl-2-acetylglycerophosphocholine EsteraseDcx protein, mouseDoublecortin Domain ProteinsDoublecortin ProteinGlucoseHistonesMicroRNAsMicrotubule-Associated ProteinsMirn200 microRNA, mouseMirn466 microRNA, mouseNeuropeptidesPafah1b1 protein, mouse

Identifiers

PMID23776576
PMCPMC3679101

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Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.