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BELTRAME Jimena Soledad

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Título:

The Interaction between Endovascular Human Trophoblast and Endothelial Cells Is Regulated in vitro by Lysophosphatidic Acid.

Autor/es:

BELTRAME, JS; SCOTTI, L; SORDELLI, MS; CAÑUMIL, VA; FRANCHI, ANA M; PARBORELL, F; RIBEIRO MARÍA LAURA

Lugar:

París

Reunión:

Congreso; Society for Reproductive Investigation; 2019

Resumen:

Spiralartery remodeling at the maternal-fetal interface is crucial for successfulpregnancy and requires the interaction between first trimester trophoblast andendothelial cells of the maternal vessels. However, the precise mechanism ofthis dialogue has yet to be determined. Previously, we reported that lysophosphatidicacid (LPA), a bioactive lipid, promotes angiogenesis of rat implantation sitesand acquisition of human first trimester trophoblast endovascular phenotype. Thecurrent study investigated whether LPA modulates in vitro trophoblast-endothelial crosstalk. HTR-8/SVneotrophoblast cell line (H8) were seeded on top of Geltrex, incubated with LPA orLPA+NS-398 (selective cyclooxygenase-2 inhibitor), LPA+1400W (selective induciblenitric oxide synthase inhibitor) or LPA+IL-6 neutralizing antibody and assayedfor tube formation to model the acquisition of trophoblast endovascularphenotype. Supernatants were collected and used as conditioned media (CM). Totest trophoblast-endothelial crosstalk, the endothelial cell line EA.hy926 wasincubated with trophoblast CM. EA.hy926 apoptosis (TUNEL assay) and migration(wound healing) were evaluated. IL-6 mRNA levels (qPCR) and MMPs activities(zymography) were determined in H8. CM fromLPA-induced tubulogenesis stimulated endothelial cells migration p<0.05 and did not modify apoptosis. However,LPA added directly to EA.hy926 did not affect endothelial cells migration compared to control-CM. Soluble factorsderived from cyclooxygenase-2 and IL-6 pathways were involved in H8 - EA.hy926interaction under LPA effect. Moreover, LPA increased IL-6 mRNA levels bycyclooxygenase-2 pathway in H8 cells p 0.05. Finally, MMP-2and MMP-9 activities in H8 supernatants were triggered by LPA p 0.05.Collectively,LPA promotes trophoblast-endothelial crosstalk in vitro and induces the releaseof trophoblast soluble factors that stimulate endothelial cells migrationwithout changes in apoptosis. The evidence presented here provides new insightsabout an active role of LPA as a lipid mediator regulating vascular adaptationsat the maternal-fetal interface.

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