Decrease in lipid levels of syncytiotrophoblast micro-particles reduced their potential to inhibit endothelial cell proliferation.
BACKGROUND
Preeclampsia is characterized by damage to the maternal endothelium that has been suggested to be mediated in part by elevated shedding of inflammatory placental syncytiotrophoblast micro-particles (STBM) into the maternal circulation. Previously, we have shown that STBM, prepared by three different methods: mechanical dissection, in vitro placental explants culture and perfusion of placenta, can inhibit endothelial cell proliferation. Only mechanically prepared STBM induced apoptosis in the endothelial cells. Now, we have examined lipid levels in the three STBM preparations and their differential responses on endothelial cells.


METHODS
We examined the lipid levels in the three STBM preparations using thin layer chromatography. Furthermore, the effects of reduced lipid levels in the three STBM preparations using the pharmacological agent methyl-beta-cyclodextrin were examined on endothelial cell proliferation and apoptosis.


RESULTS
Among the three STBM preparations, mechanical STBM contained highest levels of lipids. The reduction in lipid levels in mechanical STBM reduced their potential to inhibit human umbilical vein endothelial cells (HUVEC) proliferation and blocked their potential to induce apoptosis. No similar effect was observed following lipid reduction in the two other STBM preparations.


CONCLUSIONS
As it has been suggested that mechanically derived STBM may more closely resemble placental micro-particles generated in preeclampsia, our data suggest that lipid content may play a role in the anti-endothelial defects present in this disease.
Gupta
Anurag Kumar
AK
Laboratory for Prenatal Medicine, University Women's Hospital/Department of Research, University Hospital, Hebelstrasse, 20, 4031, Basel, Switzerland. gkumar@uhbs.ch
Holzgreve
Wolfgang
W
Hahn
Sinuhe
S
D017209:Apoptosis; D049109:Cell Proliferation; D002478:Cells, Cultured; D002855:Chromatography, Thin Layer; D042783:Endothelial Cells / Q000502:physiology; D006801:Humans; D050356:Lipid Metabolism; D014327:Trophoblasts / Q000378:metabolism*; D014471:Umbilical Veins / Q000166:cytology; D047392:beta-Cyclodextrins / Q000494:pharmacology
D047392:beta-Cyclodextrins; C108732:methyl-beta-cyclodextrin