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Autoantibodies Isolated from Patients with Preeclampsia Induce Soluble Endoglin Production from Trophoblast Cells Via Interactions with Angiotensin II Type 1 Receptor
Author(s) -
Kobayashi Yusuke,
Yamamoto Tatsuo,
Chishima Fumihisa,
Takahashi Hideki,
Suzuki Manami
Publication year - 2015
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12340
Subject(s) - preeclampsia , losartan , trophoblast , endoglin , medicine , endocrinology , receptor , autoantibody , angiotensin ii , renin–angiotensin system , chemistry , andrology , biology , fetus , antibody , placenta , immunology , pregnancy , microbiology and biotechnology , genetics , stem cell , cd34 , blood pressure
Problem This study investigated whether angiotensin II type 1 receptor agonistic autoantibodies ( AT 1 ‐ AA s) mediate the increased release of soluble endoglin (s E ng) 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 I g G derived from these sera, and the s E ng protein and m RNA expression levels were measured in the supernatants. We also determined the effects of the AT 1 ‐ AA s on these cells following treatment with an AT 1 receptor antagonist (losartan). Results Compared with the I g G isolated from the women with normal pregnancies, treatments of the preeclamptic patients markedly increased s E ng production and m RNA expression in trophoblast cells. Co‐treatment with losartan significantly attenuated the release of s E ng and s E ng m RNA expression in the trophoblast cells. Conclusion AT 1 ‐ AA s may be related to the increased release of s E ng observed during preeclampsia and may play important roles in the pathology of this disorder.