Evidence map›Paper›PMID 29489902›Full record

ArticlePloS one2018

Effects of human interleukins in the transgenic gene reporter cell lines IZ-VDRE and IZ-CYP24 designed to assess the transcriptional activity of vitamin D receptor.

Iveta Bartonkova, Enikoe Kallay, Zdenek Dvorak

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
0.2field-weighted citation impact, top 49% 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

3 citing papers in PubMed, 3 citations in OpenAlex.

  1. Review
  2. Article
  3. 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

3 authors at 2 institutions in 2 countries.

Iveta BartonkovaDepartment of Cell Biology and Genetics, Faculty of Science, Palacky University, Olomouc, Czech Republic.
Enikoe KallayDepartment of Pathophysiology and Allergy Research, Medical University of Vienna, Vienna, Austria.
Zdenek DvorakDepartment of Cell Biology and Genetics, Faculty of Science, Palacky University, Olomouc, Czech Republic.ORCID 0000-0002-3938-3585
Palacký University Olomouc · CZMedical University of Vienna · AT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The role of vitamin D receptor (VDR) in immune responses has been broadly studied and it has been shown that activated VDR alters the levels of some interleukins (ILs). In this study, we studied the opposite, i.e. whether 13 selected pro-inflammatory and anti-inflammatory ILs influence the transcriptional activity of human VDR. The experimental models of choice were two human stably transfected gene reporter cell lines IZ-VDRE and IZ-CYP24, which were designed to evaluate the transcriptional activity of VDR. The gene reporter assays revealed inhibition of calcitriol-induced luciferase activity by IL-4 and IL-13, when 1 ng/mL of these two compounds decreased the effect of calcitriol down to 60% of the control value. Consistently, calcitriol-induced expression of CYP24A1 mRNA was also significantly decreased by IL-4 and IL-13. The expression of VDR and CYP27B1 mRNAs was not influenced by any of the 13 tested ILs. These data suggest possible cross-talk between the VDR signalling pathway and IL-4- and IL-13-mediated cell signalling.

Indexed as

25-Hydroxyvitamin D3 1-alpha-HydroxylaseCell LineGenes, ReporterHumansInterleukinsReceptors, CalcitriolTranscription, GeneticTransfectionTransgenesVitamin D3 24-Hydroxylase25-Hydroxyvitamin D3 1-alpha-HydroxylaseInterleukinsReceptors, CalcitriolVitamin D3 24-Hydroxylase

Identifiers

PMID29489902
PMCPMC5831414
OpenAlexW2793380721

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.