ArticleScientific reports2018
Role of the Macrophage Migration Inhibitory Factor (MIF) in the survival of first trimester human placenta under induced stress conditions.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 20 citations in OpenAlex.
- TRAF3 as a potential diagnostic biomarker for recurrent pregnancy loss: insights from single-cell transcriptomics and machine learning.BMC pregnancy and childbirth · 2025Article
- MIF Increases sFLT1 Expression in Early Uncomplicated Pregnancy and Preeclampsia.International journal of molecular sciences · 2023Article
- Review
- A Comparative Review of Pregnancy and Cancer and Their Association with Endoplasmic Reticulum Aminopeptidase 1 and 2.International journal of molecular sciences · 2023Review
- Spatial transcriptomic profiles of mouse uterine microenvironments at pregnancy day 7.5†.Biology of reproduction · 2022Article
- Role of the Macrophage Migration Inhibitory Factor in the Pathophysiology of Pre-Eclampsia.International journal of molecular sciences · 2021Review
- Influence of Gestational Hormones on the Bacteria-Induced Cytokine Response in Periodontitis.Mediators of inflammation · 2021Review
- Article
- Recruitment of MAIT Cells to the Intervillous Space of the Placenta by Placenta-Derived Chemokines.Frontiers in immunology · 2019Article
- Macrophage migration inhibitory factor is involved in endovascular trophoblast cell functionEXCLI journal · 2019Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Macrophage Migration Inhibitory Factor (MIF) is a multifunctional molecule highly secreted by human placenta mainly in the early phases of pregnancy. Studies in different cells show that MIF is a pro-survival factor by binding to its receptor CD74. By using the in vitro model of placental explants from first trimester pregnancy, we investigated the role of MIF in the survival of placental cells under induced stress conditions that promote apoptosis or mimic the hypoxia/re-oxygenation (H/R) injury that placenta could suffer in vivo. We demonstrated that recombinant MIF (rMIF) treatment was able to reduce caspase-3 activation when cultures were challenged with the apoptosis-inducer Carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (FCCP) while, in the cultures exposed to H/R, the treatment with rMIF did not show any effect. However, a significant increase in caspase-3 and caspase-8 activation was found when H/R-exposed cultures, were treated with anti-MIF or anti-CD74 antibody. We also observed that under H/R, a significant amount of endogenous MIF was released into the medium, which could account for the lack of effect of rMIF added to the cultures. Our results demonstrate for the first time that the MIF/CD74 axis contributes to maintain trophoblast homeostasis, by preventing abnormal apoptotic death.
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