Evidence map›Paper›PMID 27981756›Full record

ArticleCell proliferation2017

Maternal diabetes modulates offspring cell proliferation and apoptosis during odontogenesis via the TLR4/NF-κB signalling pathway.

Guoqing Chen, Wenhua Sun, Yan Liang, Tian Chen, Weihua Guo, Weidong Tian

Open access · bronzeAbstract read
In one paragraph

Article in Cell proliferation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

18 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Article
  9. Heat Shock Proteins in Tooth Development and Injury Repair.International journal of molecular sciences · 2023
    Review
  10. Review
  11. Article
  12. Review
  13. Article
  14. Article
  15. Article
  16. Article
  17. World journal of gastroenterology · 2017
    Article
  18. Article
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

6 authors at 2 institutions in 1 country.

Guoqing ChenState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China.
Wenhua SunState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China.
Yan LiangState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China.
Tian ChenState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China.
Weihua GuoState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China.
Weidong TianState Key Laboratory of Oral Diseases, West China College of Stomatology, Sichuan University, Chengdu, China.
State Key Laboratory of Oral DiseasesSichuan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectivesMaternal gestational diabetes leads to an adverse in utero environment and increases the risk of malformations during embryo organogenesis. In the present study, we analysed the effects of maternal diabetes on tooth germ cell proliferation and apoptosis in offspring, and investigated their underlying mechanisms. MATERIALS AND

methodsA rat model of maternal diabetes was induced by intraperitoneal injection of streptozotocin and the pregnant rats were divided into three groups: controls, the diabetic group and diabetic group with insulin treatment. Offspring of the three groups were collected and cell proliferation and apoptosis in tooth germs were analysed. Primary dental papilla cells and dental epithelial stem cells were isolated and treated with high glucose in vitro, in an attempt to simulate maternal diabetes-induced hyperglycaemia in vivo.

resultsMaternal diabetes significantly affected cell proliferation and apoptosis in offspring tooth germs. The TLR4/NF-ĸB signalling pathway was activated in the tooth germs of offspring of diabetic dams. High glucose treatment activated the TLR4/NF-ĸB signalling pathway in primary dental papilla cells and dental epithelial stem cells in vitro, resulting in suppression of cell proliferation and enhancement of apoptosis. TLR4 knockdown significantly reduced adverse effects induced by high glucose treatment.

conclusionsMaternal gestational diabetes significantly impaired dental epithelial and mesenchymal cell proliferation and apoptosis in offspring, possibly by activation of the TLR4/NF-ĸB signalling pathway.

Indexed as

ApoptosisCell ProliferationOdontogenesisSignal TransductionAnimalsCells, CulturedDiabetes, GestationalFemaleInjections, IntraperitonealInsulinNF-kappa BPregnancyRatsStreptozocinToll-Like Receptor 4InsulinNF-kappa BStreptozocinTlr4 protein, ratToll-Like Receptor 4apoptosiscell proliferationmaternal diabetesTLR4/NF-ĸB signallingtooth development

Identifiers

PMID27981756
PMCPMC6529139
OpenAlexW2564917989

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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.