[Pre-eclampsia--endothelial damage of endothelial activation?].
There is considerable evidence that endothelial damage, followed by the release of vasoactive substances contributes to the pathophysiology of preeclampsia. Because of controversial experiences in literature we wanted to evaluate the potential cytotoxic effect of preeclamptic sera on cultured endothelial cells. Therefore cultured human umbilical vein endothelial cells (HUVEC) were stimulated with sera obtained from preeclamptic patients, while sera from normotensive pregnant and nonpregnant women served as controls. To prove the viability of these cells we performed ethidiumbromide/acridinorange immunostaining and determined t-PA/PAI-1 release into the supernatant. These experiments could not show any cytotoxic effect on endothelial cells. In ongoing studies we measured the concentrations of adhesion molecules, markers of endothelial activation, in maternal sera, in the supernatant of cultured endothelial cells, and on cell surface after stimulation with the above mentioned sera. In the supernatant we couldn't determine any different concentrations of adhesion molecules after stimulation with the different sera, but using immunofluorescence-microscopy an increased concentration of those molecules could be detected on the endothelial surface after stimulation with preeclamptic sera than compared to sera from normotensive controls. In conclusion, our experiments support the hypothesis that sera from preeclamptic women may cause endothelial activation.
Heyl
W
W
Universitätsfrauenklinik für Gynäkologie und Geburtshilfe, RWTH Aachen.
Faridi
A
A
Reister
F
F
Rath
W
W
D015815:Cell Adhesion Molecules / Q000502:physiology; D002470:Cell Survival / Q000502:physiology; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000503:physiopathology*; D005260:Female; D006801:Humans; D007231:Infant, Newborn; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D012016:Reference Values
D015815:Cell Adhesion Molecules