Evidence map›Paper›PMID 28094306›Full record

ArticleScientific reports2017

Maternal diabetes modulates dental epithelial stem cells proliferation and self-renewal in offspring through apurinic/apyrimidinicendonuclease 1-mediated DNA methylation.

Guoqing Chen, Jie Chen, Zhiling Yan, Ziyue Li, Mei Yu, Weihua Guo, Weidong Tian

Open access · goldAbstract read
In one paragraph

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 10 papers.

0numbers the graph read from it
0cells of the map it votes in
10citing papers in PubMed
1.5field-weighted citation impact, top 19% of its field
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

10 citing papers in PubMed, 20 citations in OpenAlex.

  1. Trial
  2. Article
  3. Review
  4. Article
  5. Article
  6. Review
  7. Article
  8. Stress Marks on the Genome: Use or Lose?International journal of molecular sciences · 2019
    Review
  9. Article
  10. Cardiac Cell Senescence and Redox Signaling.Frontiers in cardiovascular medicine · 2017
    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 at 2 institutions in 1 country.

Guoqing ChenState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, 610041, P. R. China.
Jie ChenState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, 610041, P. R. China.
Zhiling YanState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, 610041, P. R. China.
Ziyue LiState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, 610041, P. R. China.
Mei YuState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, 610041, P. R. China.
Weihua GuoState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, 610041, P. R. China.
Weidong TianState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, 610041, P. R. China.
Sichuan University · CNState Key Laboratory of Oral Diseases

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maternal gestational diabetes mellitus (GDM) has many adverse effects on the development of offspring. Aberrant DNA methylation is a potential mechanism associated with these effects. However, the effects of GDM on tooth development and the underlying mechanisms have not been thoroughly investigated. In the present study, a GDM rat model was established and incisor labial cervical loop tissue and dental epithelial stem cells (DESCs) were harvested from neonates of diabetic and control dams. GDM significantly suppressed incisor enamel formation and DESCs proliferation and self-renewal in offspring. Gene expression profiles showed that Apex1 was significantly downregulated in the offspring of diabetic dams. In vitro, gain and loss of function analyses showed that APEX1 was critical for DESCs proliferation and self-renewal and Oct4 and Nanog regulation via promoter methylation. In vivo, we confirmed that GDM resulted in significant downregulation of Oct4 and Nanog and hypermethylation of their promoters. Moreover, we found that APEX1 modulated DNA methylation by regulating DNMT1 expression through ERK and JNK signalling. In summary, our data suggest that GDM-induced APEX1 downregulation increased DNMT1 expression, thereby inhibiting Oct4 and Nanog expression, through promoter hypermethylation, resulting in suppression of DESCs proliferation and self-renewal, as well as enamel formation.

Indexed as

Diabetes, GestationalDNA MethylationAnimalsBlood GlucoseCell ProliferationCell Self RenewalDental Enamel HypoplasiaDNA-(Apurinic or Apyrimidinic Site) LyaseDNA (Cytosine-5-)-Methyltransferase 1FemaleGene Expression RegulationMAP Kinase Signaling SystemMorphogenesisNanog Homeobox ProteinOctamer Transcription Factor-3PregnancyApex1 protein, ratBlood GlucoseDNA-(Apurinic or Apyrimidinic Site) LyaseDNA (Cytosine-5-)-Methyltransferase 1Dnmt1 protein, ratNanog Homeobox ProteinOctamer Transcription Factor-3

Identifiers

PMID28094306
PMCPMC5240105
OpenAlexW2576941036

What OpenQuestion holds

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LicenceCC BY
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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.