Macrophage migration inhibitory factor is involved in endovascular trophoblast cell function in vitro

Authors

  • Aleksandra Vilotic Laboratory for Biology of Reproduction, Institute for the Application of Nuclear Energy, INEP, University of Belgrade, Banatska 31b, 11080 Belgrade, Serbia
  • Milica Jovanovic Krivokuca Laboratory for Biology of Reproduction, Institute for the Application of Nuclear Energy, INEP, University of Belgrade, Banatska 31b, 11080 Belgrade, Serbia; Tel. +381 11 316 90 58, Fax. +381 11 2618 724, E-mail: milicaj@inep.co.rs
  • Ivana Stefanoska Laboratory for Biology of Reproduction, Institute for the Application of Nuclear Energy, INEP, University of Belgrade, Banatska 31b, 11080 Belgrade, Serbia
  • Svetlana Vrzic Petronijevic Clinic of Obstetrics and Gynecology, Clinical Center of Serbia, Koste Todorovića 26, 11000 Belgrade, Serbia
  • Milos Petronijevic Clinic of Obstetrics and Gynecology, Clinical Center of Serbia, Koste Todorovića 26, 11000 Belgrade, Serbia
  • Ljiljana Vicovac Laboratory for Biology of Reproduction, Institute for the Application of Nuclear Energy, INEP, University of Belgrade, Banatska 31b, 11080 Belgrade, Serbia

DOI:

https://doi.org/10.17179/excli2019-1630

Keywords:

trophoblast, HTR-8/SVneo, HUVEC, N-cadherin

Abstract

Macrophage migration inhibitory factor (MIF) is a multifunctional cytokine abundantly present at the feto-maternal interface proposed to play a role in establishment of pregnancy. We have previously shown that pharmacological inhibition of enzymatic activity of MIF decreases extravillous trophoblast invasion and migration in vitro. This study aimed to further elucidate potential role of endogenous trophoblast MIF, and to assess its importance for endovascular trophoblast cell function in particular. Attenuation of MIF by siRNA reduced HTR-8/SVneo cell invasion through Matrigel (59 % of control), expression of integrin α1 (86 % of control) and levels of MMP2 and MMP9 (87 % and 57 % of control, respectively). MIF specific siRNA reduced the ability of HTR-8/SVneo to differentiate in to endothelial-like phenotype, as determined by Matrigel tube formation assay. The total tube length was decreased to 68.6 %, while the number of branching points was reduced to 57.8 % of control. HTR-8/SVneo cell capacity to integrate into HUVEC monolayers was reduced by knock-down of MIF. This could be partly caused by reduced N-cadherin expression to 63 % of control, which decreased with knock-down of MIF, as the expression of this protein was recently shown essential for trophoblast-endothelial interaction. These novel findings indicate a novel role for trophoblast MIF in spiral artery remodeling process.

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Published

2019-10-31

How to Cite

Vilotic, A., Jovanovic Krivokuca, M., Stefanoska, I., Vrzic Petronijevic, S., Petronijevic, M., & Vicovac, L. (2019). Macrophage migration inhibitory factor is involved in endovascular trophoblast cell function in vitro. EXCLI Journal, 18, 1007–1018. https://doi.org/10.17179/excli2019-1630

Issue

Vol. 18 (2019)

Section

Original articles

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