Autoantibodies isolated from patients with preeclampsia induce soluble endoglin production from trophoblast cells via interactions with angiotensin II type 1 receptor.

PROBLEM: This study investigated whether angiotensin II type 1 receptor agonistic autoantibodies (AT1 -AAs) mediate the increased release of soluble endoglin (sEng) in women with preeclampsia. METHOD OF STUDY: Serum samples were obtained from women with normal pregnancies or with preeclampsia. Human first-trimester trophoblast cells were cultured with purified IgG derived from these sera, and the sEng protein and mRNA expression levels were measured in the supernatants. We also determined the effects of the AT1 -AAs on these cells following treatment with an AT1 receptor antagonist (losartan).
RESULTS: Compared with the IgG isolated from the women with normal pregnancies, treatments of the preeclamptic patients markedly increased sEng production and mRNA expression in trophoblast cells. Co-treatment with losartan significantly attenuated the release of sEng and sEng mRNA expression in the trophoblast cells.
CONCLUSION: AT1 -AAs may be related to the increased release of sEng observed during preeclampsia and may play important roles in the pathology of this disorder.