Evidence map›Paper›PMID 25165878›Full record

ArticleCell death & disease2014

Influence of relative NK-DC abundance on placentation and its relation to epigenetic programming in the offspring.

N Freitag, M V Zwier, G Barrientos, I Tirado-González, M L Conrad, M Rose, S A Scherjon, T Plösch, S M Blois

Open access · goldAbstract read
In one paragraph

Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.5field-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

17 citing papers in PubMed, 25 citations in OpenAlex.

  1. Review
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  7. Sex and Exposure to Postnatal Chlorpyrifos Influence the Epigenetics of Feeding-Related Genes in a TransgenicInternational journal of environmental research and public health · 2020
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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 3 institutions in 2 countries.

N FreitagLaboratory of Reproductive Medicine, Medicine University of Berlin, Charité Centre 12 Internal Medicine and Dermatology, Berlin, Germany.
M V ZwierCenter for Liver, Department of Pediatrics, University Medical Center Groningen, University of Groningen, Digestive and Metabolic Diseases, Groningen, The Netherlands.
G BarrientosLaboratory of Reproductive Medicine, Medicine University of Berlin, Charité Centre 12 Internal Medicine and Dermatology, Berlin, Germany.
I Tirado-GonzálezLaboratory of Reproductive Medicine, Medicine University of Berlin, Charité Centre 12 Internal Medicine and Dermatology, Berlin, Germany.
M L ConradLaboratory of Reproductive Medicine, Medicine University of Berlin, Charité Centre 12 Internal Medicine and Dermatology, Berlin, Germany.
M RoseLaboratory of Reproductive Medicine, Medicine University of Berlin, Charité Centre 12 Internal Medicine and Dermatology, Berlin, Germany.
S A ScherjonDepartment of Obstetrics and Gynaecology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
T PlöschDepartment of Obstetrics and Gynaecology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands.
S M BloisLaboratory of Reproductive Medicine, Medicine University of Berlin, Charité Centre 12 Internal Medicine and Dermatology, Berlin, Germany.
Humboldt-Universität zu Berlin · DEFreie Universität Berlin · DEUniversity Medical Center Groningen · NL

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Normal placentation relies on an efficient maternal adaptation to pregnancy. Within the decidua, natural killer (NK) cells and dendritic cells (DC) have a critical role in modulating angiogenesis and decidualization associated with pregnancy. However, the contribution of these immune cells to the placentation process and subsequently fetal development remains largely elusive. Using two different mouse models, we here show that optimal placentation and fetal development is sensitive to disturbances in NK cell relative abundance at the fetal-maternal interface. Depletion of NK cells during early gestation compromises the placentation process by causing alteration in placental function and structure. Embryos derived from NK-depleted dams suffer from intrauterine growth restriction (IUGR), a phenomenon that continued to be evident in the offspring on post-natal day 4. Further, we demonstrate that IUGR was accompanied by an overall reduction of global DNA methylation levels and epigenetic changes in the methylation of specific hepatic gene promoters. Thus, temporary changes within the NK cell pool during early gestation influence placental development and function, subsequently affecting hepatic gene methylation and fetal metabolism.

Indexed as

Epigenesis, GeneticAnimalsDendritic CellsDNA MethylationFemaleFetal Growth RetardationHeparin-binding EGF-like Growth FactorKiller Cells, NaturalMiceMice, Inbred C57BLPlacentaPlacentationPregnancyUterusHeparin-binding EGF-like Growth Factor

Identifiers

PMID25165878
PMCPMC4454325
OpenAlexW2035389321

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.