Evidence map›Paper›PMID 25415335›Full record

ArticleReproductive sciences (Thousand Oaks, Calif.)2015

Hypoxia-Mediated Soluble Fms-Like Tyrosine Kinase 1 Increase Is Not Attenuated in Interleukin 6-Deficient Mice.

Sarah Appel, Eva-Maria Turnwald, Janina Ankerne, Maria Wohlfarth, Jan Appel, Eva Rother, Ruth Janoschek, Miguel A Alejandre Alcazar, Markus Schnare, Udo Meißner and 1 more

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 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact, top 86% 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, 7 citations in OpenAlex.

  1. Gestational Factors throughout Fetal Neurodevelopment: The Serotonin Link.International journal of molecular sciences · 2020
    Review
  2. Article
  3. Preeclampsia link to gestational hypoxia.Journal of developmental origins of health and disease · 2019
    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

11 authors at 2 institutions in 1 country.

Sarah AppelDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany sarah.appel@uk-koeln.de.
Eva-Maria TurnwaldDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany.
Janina AnkerneDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany.
Maria WohlfarthDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany.
Jan AppelDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany.
Eva RotherDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany.
Ruth JanoschekDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany.
Miguel A Alejandre AlcazarDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany.
Markus SchnareInstitute for Immunology, University of Marburg, Marburg, Germany.
Udo MeißnerHainstrasse 20, 96047 Bamberg, Germany.
Jörg DötschDepartment of Pediatrics and Adolescent Medicine, University of Cologne, Cologne, Germany.
University of Cologne · DEPhilipps University of Marburg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The soluble fms-like tyrosine kinase 1 (sFlt-1), known to be increased in the serum of preeclamptic patients, is a relevant factor in causing maternal symptoms like hypertension and proteinuria. In this study, we aimed to reveal whether hypoxia is a cause of increased sFlt-1 levels and inflammation markers in vivo and whether these symptoms can be attenuated by interleukin 6 (IL-6) depletion. For this purpose, pregnant wild-type (wt) mice or IL-6(-/-) mice on embryonic day 16 were placed under either normoxic (20.9% oxygen) or hypoxic (6% oxygen) conditions for 6 hours. This led to a rise of sFlt-1 levels in maternal serum, independent of the IL-6 status of the dam. Increased maternal sFlt-1 serum levels were, however, not due to an increase in sFlt-1 messenger RNA levels in the placenta. Moreover, there was no increase in inflammatory markers in neither wt mice nor IL-6(-/-) mice. This suggests that hypoxia alone does not contribute to the induction of an inflammatory placenta. Also, the hypoxia-induced rise in sFlt-1 levels seems not to be mediated by IL-6 in vivo.

Indexed as

AnimalsDisease Models, AnimalFemaleGestational AgeHypoxiaHypoxia-Inducible Factor 1, alpha SubunitInflammationInterleukin-6Mice, Inbred C57BLMice, KnockoutPlacentaPregnancyUp-RegulationVascular Endothelial Growth Factor Receptor-1Flt1 protein, mouseHif1a protein, mouseHypoxia-Inducible Factor 1, alpha SubunitInterleukin-6interleukin-6, mouseVascular Endothelial Growth Factor Receptor-1hypoxiaplacentasFlt-1

Identifiers

PMID25415335
PMCPMC4502805
OpenAlexW2100495760

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.