Evidence map›Paper›PMID 29786111›Full record

ArticleInternational journal of molecular medicine2018

High glucose suppresses the viability and proliferation of HTR‑8/SVneo cells through regulation of the miR‑137/PRKAA1/IL‑6 axis.

Hai-Yan Peng, Ming-Qing Li, Hua-Ping Li

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

31 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
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  11. The Role of Ferroptosis in Placental-Related Diseases.Reproductive sciences (Thousand Oaks, Calif.) · 2023
    Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Iron Metabolism and Ferroptosis in Physiological and Pathological Pregnancy.International journal of molecular sciences · 2022
    Review
  17. Article
  18. Article
  19. Article
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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

3 authors at 2 institutions in 1 country.

Hai-Yan PengDepartment of Gynecology and Obstetrics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Ming-Qing LiLaboratory for Reproductive Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Obstetrics and Gynecology Hospital of Fudan University, Shanghai 200011, P.R. China.
Hua-Ping LiDepartment of Gynecology and Obstetrics, Shanghai Jiao Tong University Affiliated Sixth People's Hospital, Shanghai 200233, P.R. China.
Shanghai Sixth People's Hospital · CNObstetrics and Gynecology Hospital of Fudan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The aim of the present study was to investigate the mechanism underlying the high glucose (HG)‑associated regulation of HTR‑8/SVneo cell viability and proliferation during gestational diabetes mellitus (GDM), and to verify the association of microRNA (miR)‑137, protein kinase AMP‑activated catalytic subunit α1 (PRKAA1) and interlukin‑6 (IL‑6). miR‑137‑overexpressing and negative control HTR‑8/SVneo cells were established by lentiviral vector infection. Cell Counting Kit‑8 and colony formation assays were used to analyze the viability and proliferation of HTR‑8/SVneo cells. Reverse transcription‑quantitative polymerase chain reaction analysis was used to determine the transcriptional activity of miR‑137, PRKAA1 and Il‑6, and ELISA and western blot analysis were used to measure the protein levels of IL‑6 and PRKAA1, respectively. It was demonstrated that PRKAA1 was decreased in the placental tissues of women with GDM and HG‑treated HTR‑8/SVneo cells, and that HG upregulated miR‑137 and IL‑6 in trophoblasts. The overexpression of miR‑137 decreased levels of PRKAA1 and increased levels of IL‑6 in the HTR‑8/SVneo cells. An inhibitor of PRKAA1 promoted the secretion of IL‑6, whereas an agonist of PRKAA1 suppressed the production of IL‑6. HG treatment and the overexpression of miR‑137 reduced the viability and proliferation of HTR‑8/SVneo cells in vitro, whereas the activation of PRKAA1 or incubation with IL‑6 antibody reversed these effects. Overall, it was concluded that HG suppressed the viability and proliferation of trophoblast cells through the miR‑137/PRKAA1/IL‑6 axis, which may contribute to pathological changes of placental tissues in GDM.

Indexed as

Cell SurvivalAdultAMP-Activated Protein KinasesCell LineCell ProliferationFemaleGene Expression RegulationGlucoseHumansInterleukin-6MicroRNAsSignal TransductionTrophoblastsYoung AdultAMP-Activated Protein KinasesGlucoseInterleukin-6MicroRNAsMIRN137 microRNA, humanPRKAA1 protein, human

Identifiers

PMID29786111
PMCPMC6034938
OpenAlexW2804400350

What OpenQuestion holds

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LicenceCC BY-NC-ND
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Registered trials

None linked

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.