Evidence map›Paper›PMID 39561117›Full record

ArticleBiology of reproduction2025

Visfatin exerts an anti-proliferative and pro-apoptotic effect in the human placenta cells†.

Monika Dawid, Karolina Pich, Natalia Respekta-Długosz, Wiktoria Gieras, Małgorzata Opydo, Tomasz Milewicz, Pascal Froment, Joëlle Dupont, Agnieszka Rak

Abstract read
In one paragraph

Article in Biology of reproduction, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
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

1 citing paper in PubMed.

  1. 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

9 authors.

Monika DawidLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University in Krakow, Poland.
Karolina PichLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University in Krakow, Poland.
Natalia Respekta-DługoszLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University in Krakow, Poland.
Wiktoria GierasLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University in Krakow, Poland.
Małgorzata OpydoLaboratory of Experimental Hematology, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University in Krakow, Poland.
Tomasz MilewiczDepartment of Gynecological Endocrinology, Faculty of Medicine, Jagiellonian University Medical College, Poland.
Pascal FromentINRAE, Unité Physiologie de la Reproduction et des Comportements, France.
Joëlle DupontINRAE, Unité Physiologie de la Reproduction et des Comportements, France.
Agnieszka RakLaboratory of Physiology and Toxicology of Reproduction, Institute of Zoology and Biomedical Research, Faculty of Biology, Jagiellonian University in Krakow, Poland.

Funding

Ministry of Education and Science DI2019 0110 49Ministry of Science and Higher Education DI2019 0110 49
6 · The paper itself

Abstract

Visfatin regulates energy homeostasis, metabolism, inflammation, and reproduction via the hypothalamus-pituitary-ovary axis. Our previous study showed the visfatin gene and protein expression in the human placenta. This study aimed to investigate the in vitro effect of visfatin on the proliferation and apoptosis of placental JEG-3 and BeWo cells but also in villous explants collected from normal pregnancies and complicated by intrauterine growth restriction (IUGR), preeclampsia (PE), and gestational diabetes mellitus (GDM). We studied placenta cells viability, proliferation, cell cycle, proliferation/apoptotic factors and insulin receptor (INSR) expression, DNA fragmentation, CASP3/7 activity, and phosphorylation of ERK1/2, AKT, AMPKα, STAT3 with their involvement after pharmacological inhibition in visfatin action on proliferation and apoptosis. Visfatin (1, 10, 100 ng/mL) decreased the viability and proliferation of JEG-3 after 48 h, and a similar effect was observed via co-administration of visfatin (10 ng/mL) and insulin (10 ng/mL) in JEG-3 and BeWo after 48 h and 72 h, respectively. Visfatin reduced the transition from the G2/M phase, and expression of PCNA or cyclins D, E, A, and B in JEG-3 and PCNA in normal, IUGR, PE, and GDM placentas. It increased DNA fragmentation, CASP3/7 activity, P53, BAX/BCL2, CASP9, CASP 8, CASP3 levels in BeWo, and CASP3 expression in tested placentas. Furthermore, visfatin modulated INSR, ERK1/2, AKT, AMPKα, and STAT3 expression in JEG-3 and BeWo, and its anti-proliferative and pro-apoptotic effects occurred via mentioned factors. In conclusion, visfatin, by affecting the proliferation and apoptosis of human placenta cells, may be an important factor in the development and function of the organ.

Indexed as

ApoptosisCell ProliferationCytokinesNicotinamide PhosphoribosyltransferasePlacentaCell SurvivalDiabetes, GestationalFemaleFetal Growth RetardationHumansPre-EclampsiaPregnancyCytokinesNicotinamide Phosphoribosyltransferasenicotinamide phosphoribosyltransferase, humanapoptosisplacentapregnancy disordersproliferationsignaling pathwaysvisfatin

Identifiers

PMID39561117
PMCPMC11833490

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Registered trials

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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.