Evidence map›Paper›PMID 24711815›Full record

ArticlePPAR research2014

PPAR- γ Regulates Trophoblast Differentiation in the BeWo Cell Model.

Khrystyna Levytska, Sascha Drewlo, Dora Baczyk, John Kingdom

Open access · goldAbstract read
In one paragraph

Article in PPAR research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
3.1field-weighted citation impact, top 9% 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

26 citing papers in PubMed, 42 citations in OpenAlex.

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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

4 authors at 3 institutions in 2 countries.

Khrystyna LevytskaResearch Centre for Women's and Infants' Health, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Room 3-904, Toronto, ON, Canada M5G 1Z5 ; Department of Laboratory Medicine and Pathobiology, University of Toronto, ON, Canada.
Sascha DrewloDepartment of Obstetrics and Gynecology, C. S. Mott Center for Human Growth and Development, Wayne State University School of Medicine, Detroit, MI, USA.
Dora BaczykResearch Centre for Women's and Infants' Health, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Room 3-904, Toronto, ON, Canada M5G 1Z5.
John KingdomResearch Centre for Women's and Infants' Health, Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, 600 University Avenue, Room 3-904, Toronto, ON, Canada M5G 1Z5 ; Department of Laboratory Medicine and Pathobiology, University of Toronto, ON, Canada ; Maternal-Fetal Medicine Division, Department of Obstetrics and Gynecology, Mount Sinai Hospital, 600 University Avenue, Room 3-904, Toronto, ON, Canada M5G 1Z5 ; Department of Obstetrics and Gynecology, University of Toronto, Toronto, ON, Canada.
Mount Sinai Hospital · CAUniversity of Toronto · CAWayne State University · US

Funding

The Role of PPARγ in Human Placental Development and PreeclampsiaR01HL128628 · NHLBI · WAYNE STATE UNIVERSITY · PI DREWLO, SASCHA · 2015 to 2019
$1.9M
NHLBI NIH HHS R01 HL128628
6 · The paper itself

Abstract

Common pregnancy complications, such as severe preeclampsia and intrauterine growth restriction, disrupt pregnancy progression and impair maternal and fetal wellbeing. Placentas from such pregnancies exhibit lesions principally within the syncytiotrophoblast (SCT), a layer in direct contact with maternal blood. In humans and mice, glial cell missing-1 (GCM-1) promotes differentiation of underlying cytotrophoblast cells into the outer SCT layer. GCM-1 may be regulated by the transcription factor peroxisome proliferator-activated receptor-gamma (PPAR- γ ); in mice, PPAR- γ promotes labyrinthine trophoblast differentiation via Gcm-1, and, as we previously demonstrated, PPAR- γ activation ameliorates disease features in rat model of preeclampsia. Here, we aimed to characterize the baseline activity of PPAR- γ in the human choriocarcinoma BeWo cell line that mimics SCT formation in vitro and modulate PPAR- γ activity to study its effects on cell proliferation versus differentiation. We report a novel negative autoregulatory mechanism between PPAR- γ activity and expression and show that blocking PPAR- γ activity induces cell proliferation at the expense of differentiation, while these remain unaltered following treatment with the agonist rosiglitazone. Gaining a deeper understanding of the role and activity of PPAR- γ in placental physiology will offer new avenues for the development of secondary prevention and/or treatment options for placentally-mediated pregnancy complications.

Identifiers

PMID24711815
PMCPMC3953466
OpenAlexW2060583339

What OpenQuestion holds

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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.