Endogenous and exogenous miR-520c-3p modulates CD44-mediated extravillous trophoblast invasion.

Autor: Takahashi H; Department of Molecular Medicine and Anatomy, Nippon Medical School, Tokyo 113-8602, Japan; Department of Obstetrics and Gynecology, Jichi Medical University, Tochigi 329-0498, Japan., Ohkuchi A; Department of Obstetrics and Gynecology, Jichi Medical University, Tochigi 329-0498, Japan., Kuwata T; Department of Obstetrics and Gynecology, Jichi Medical University, Tochigi 329-0498, Japan., Usui R; Department of Obstetrics and Gynecology, Jichi Medical University, Tochigi 329-0498, Japan., Baba Y; Department of Obstetrics and Gynecology, Jichi Medical University, Tochigi 329-0498, Japan., Suzuki H; Department of Obstetrics and Gynecology, Jichi Medical University, Tochigi 329-0498, Japan., Chaw Kyi TT; Department of Molecular Medicine and Anatomy, Nippon Medical School, Tokyo 113-8602, Japan., Matsubara S; Department of Obstetrics and Gynecology, Jichi Medical University, Tochigi 329-0498, Japan., Saito S; Department of Obstetrics and Gynecology, Faculty of Medicine, University of Toyama, Toyama 930-0194, Japan., Takizawa T; Department of Molecular Medicine and Anatomy, Nippon Medical School, Tokyo 113-8602, Japan. Electronic address: t-takizawa@nms.ac.jp.
Jazyk: angličtina
Zdroj: Placenta [Placenta] 2017 Feb; Vol. 50, pp. 25-31. Date of Electronic Publication: 2016 Dec 14.
DOI: 10.1016/j.placenta.2016.12.016
Abstrakt: Introduction: Adequate extravillous trophoblast (EVT) invasion is essential for successful placentation. Although miR-520c-3p plays an important role in CD44-mediated invasion in cancer cells, there is little information on whether miR-520c-3p is involved in the regulatory mechanisms of CD44-mediated EVT invasion.
Methods: We screened first trimester trophoblast cells and trophoblast cell lines for expression of miR-520c-3p using real-time polymerase chain reaction. The cell invasion assay was performed using EVT cell lines, HTR8/SVneo and HChEpC1b, to investigate the capability of suppressing EVT invasion by miR-520c-3p. Laser microdissection analysis was then used to determine whether miR-520c-3p was present in the first trimester decidua. Finally, the possibility of chorionic villous trophoblast (CVT)-EVT communication via exosomal miR-520c-3p was determined using an in vitro model based on BeWo exosomes and the EVT cell lines as recipient cells.
Results: The miR-520c-3p level was significantly downregulated in EVT cell lines and EVTs. Cell invasion was significantly inhibited in miR-520c-3p-overexpressing cell lines, involving a significant reduction of CD44. Laser microdissection analysis showed that miR-520c-3p in the periarterial area of the decidua was significantly higher than that in the non-periarterial area. Using an in vitro model system, BeWo exosomal miR-520c-3p was internalized into the EVT cells with subsequently reduced cell invasion via CD44 repression.
Conclusions: EVT invasion is synergistically enhanced by the reciprocal expression of endogenous miR-520c-3p and CD44. The present study supports a novel model involving a placenta-associated miRNA function in cell-cell communication in which CVT exosomal miR-520c-3p regulates cell invasion by targeting CD44 in EVTs.
(Copyright © 2016 Elsevier Ltd. All rights reserved.)
Databáze: MEDLINE
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