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Placenta. 2014 Feb;35 Suppl:S51-6. doi: 10.1016/j.placenta.2013.10.015. Epub 2013 Nov 1.

Review: putative roles for the macrophage migratory inhibitory factor at the maternal fetal interface.

Author information

1
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, SP, Brazil. Electronic address: bevilacq@usp.br.
2
Department of Life Sciences, Reproductive Physiology, University of Siena, Siena, Italy.
3
Laboratory of Histology and Embryology, Institute of Biomedical Sciences, Federal University of Uberlandia, Uberlandia, MG, Brazil.
4
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, SP, Brazil.
5
Department of Cell and Developmental Biology, Institute of Biomedical Sciences, University of São Paulo, SP, Brazil; Laboratory of Cell Biology, Stomatology Department, Dentistry School, University of São Paulo, SP, Brazil.

Abstract

Complex and dynamic networks of molecules participate in the essential interactions between maternal organism, placenta and fetus in a healthy and successful pregnancy. Macrophage migratory inhibitory factor (MIF) is one of several molecules produced at implantation sites; MIF is mostly expressed by trophoblast cells. This has led to expectations of MIF's relevance as a partner in the maternal/fetal dialog. MIF is known by its biological interactions and functional roles as an activator of innate immunity, regulating subsequent adaptive responses, which include inhibition of migration of mononuclear cells in vitro, antagonism of glucocorticoids, and regulation of expression of Toll-like receptor 4. Beyond roles in the inflammatory response, MIF can interfere with proliferative activities in different cell types, as well as with cell death pathways. This intriguing factor found at the human, porcine, ovine, bovine and rodent maternal-fetal interfaces is present in a time- and spatially-dependent manner, indicating regulatory roles in the process of embryo implantation, placental development, maintenance of pregnancy and birth. Here, we will review MIF participation in placental physiology, including new evidence for a dialog with uterine cells, and a potential role in protection of uterine decidual cells.

KEYWORDS:

AKT signaling pathway; Apoptosis; Cell survival; Decidual cells; MIF; Mdm2

PMID:
24215782
DOI:
10.1016/j.placenta.2013.10.015
[Indexed for MEDLINE]

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