Evidence map›Paper›PMID 25028176›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2015

Gestational diabetes mellitus upregulates vitamin D receptor in extravillous trophoblasts and fetoplacental endothelial cells.

Julia Knabl, Rebecca Hüttenbrenner, Stefan Hutter, Maria Günthner-Biller, Christina Riedel, Ursula Hiden, Franz Kainer, Gernot Desoye, Udo Jeschke

Open access · bronzeAbstract read
In one paragraph

Article in Reproductive sciences (Thousand Oaks, Calif.), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

12 citing papers in PubMed, 29 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Review
  5. Placental mitochondrial dysfunction with metabolic diseases: Therapeutic approaches.Biochimica et biophysica acta. Molecular basis of disease · 2021
    Review
  6. Article
  7. Article
  8. Article
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  10. Review
  11. 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

9 authors at 2 institutions in 2 countries.

Julia KnablDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany.
Rebecca HüttenbrennerDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany.
Stefan HutterDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany.
Maria Günthner-BillerDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany.
Christina RiedelDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany Institut für Soziale Pädiatrie und Jugendmedizin, Ludwig-Maximilians-Universität München, Munich, Germany.
Ursula HidenDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany Department of Obstetrics and Gynecology, Medical University Graz, Graz, Austria.
Franz KainerDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany.
Gernot DesoyeDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany Department of Obstetrics and Gynecology, Medical University Graz, Graz, Austria.
Udo JeschkeDepartment of Obstetrics and Gynecology, Ludwig-Maximilians-Universität, Munich, Germany udo.jeschke@med.uni-muenchen.de.
Ludwig-Maximilians-Universität München · DEMedical University of Graz · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveGestational diabetes mellitus (GDM) is often accompanied by low maternal vitamin D, that is, calcitriol (1,25[OH]2 vitamin D3), levels. Here, we tested the hypothesis that the placental vitamin D receptor (VDR) is regulated by calcitriol and altered in GDM with distinct changes in different placental cell types. Specifically, we aimed to localize VDR in human term placentas from normal and GDM pregnancies, to quantify its cellular expression and to study in vitro its regulation by its physiological agonist calcitriol. STUDY

designPlacental tissue slides of 80 patients (40 with GDM/40 controls) were double stained for VDR and human leukocyte antigen G to identify extravillous trophoblasts (EVTs). Staining intensity was semiquantified. Quantitative real time-polymerase chain reaction and Western blotting measured VDR messenger RNA (mRNA) and protein in decidual tissue. The trophoblast cell line BeWo was used to study in vitro VDR regulation by calcitriol (0.01, 0.1, and 1 nmol/mL).

resultsVitamin D receptor protein and mRNA levels are upregulated (P < .05) in EVT (1.8-fold) as well as in placental endothelium (5.8-fold) of patients with GDM. Expression of VDR is regulated by calcitriol in a bimodal manner: high doses (0.1 and 1 nmol/mL) caused downregulation, whereas the low dose (0.01 nmol/mL) resulted in VDR upregulation.

conclusionVitamin D receptor is upregulated in EVT and endothelium of GDM placentas. This could be due to low maternal vitamin D levels in patients with GDM because in vitro low calcitriol doses upregulate VDR in trophoblast cells.

Indexed as

AdultCalcitriolCase-Control StudiesCell Line, TumorDiabetes, GestationalDose-Response Relationship, DrugEndothelial CellsFemaleHumansPlacentaPregnancyReceptors, CalcitriolRNA, MessengerTrophoblastsUp-RegulationCalcitriolReceptors, CalcitriolRNA, MessengerVDR protein, humangestational diabetes mellitusnuclear receptortrophoblastsvitamin D receptor

Identifiers

PMID25028176
PMCPMC4352142
OpenAlexW1985061815

What OpenQuestion holds

Textmetadata
Read underepoch 390

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.