Receptor expression by JEG-3 trophoblast cells in the presence of placenta secreted factors

Abstract

Preeclampsia still remains one of the most severe pregnancy complications and is an actual problem in the obstetrics practice. At present, the joint impact of cytokines and other placenta secreted factors on trophoblast cell functional activity during preeclampsia complicated pregnancy remains unclear. The aim of the study is to estimate the surface receptors expression by trophoblast cells in the presence of placenta secreted factors during physiological pregnancy and at preeclampsia. Trophoblast cells of the JEG-3 line were incubated in the presence of supernatants obtained by cultivation of placentas from women with physiological pregnancy and with preeclampsia. Surface receptors expression by trophoblast cells was estimated by FACS Canto II flow cytometer. It was established that in the third trimester both under normal and pathological conditions, the placenta secreted factors impact on the cytokine receptor expression by trophoblast differs while the trophoblast response capacity to the migration and proliferation stimulating and inhibiting signals remains stable. JEG-3 line cells enhanced the expression of CD186, CD140a, Integrin b6, VE-cadherin, CD29, and CD140a in the case of incubation in the presence of placenta supernatants from the third-trimester pregnancy complicated with preeclampsia compared to incubation in the presence of placenta supernatants form the third trimester of physiological pregnancy.

Natural Killer Cell Derived Microvesicles Affect the Function of Trophoblast Cells

“…Thus, unlike endothelial cells, trophoblast cells are resistant to the transfer of receptors associated with the cytoplasmic membrane. The selection of trophoblast surface molecules for analysis was based on changes in their expression in the presence of inducers ( Table 1 ) [ 63 , 93 ]. The lack of influence of NK-92 cell MVs on the expression of trophoblast receptors CD54, CD105, CD126, CD130, CD181, CD119, and CD120a may be an indication in favor of both the resistance of the trophoblast cell phenotype to such an effect and the stability of the expression of these particular molecules by trophoblasts.…”