Autoantibodies Isolated from Patients with Preeclampsia Induce Soluble Endoglin Production from Trophoblast Cells Via Interactions with Angiotensin II Type 1 Receptor. (7th November 2014)

• Record Type: Journal Article
• Authors: Kobayashi, Yusuke; Yamamoto, Tatsuo; Chishima, Fumihisa; Takahashi, Hideki; Suzuki, Manami
• Is Part Of: American journal of reproductive immunology. Volume 73:Number 4(2015:Apr.)
• Page Start: 285
• Page End: 291
• Publication Date: 2014-11-07
• Subjects: Human reproduction -- Immunological aspects -- Periodicals; 616.69206
• DOI: 10.1111/aji.12340
• Languages: English
• ISSNs: 1046-7408

Abstract

<abstract abstract-type="main" id="aji12340-abs-0001"> <title> <x xml:space="preserve">Abstract</x> </title> <sec id="aji12340-sec-0001" sec-type="section"> <title>Problem</title> <p>This study investigated whether angiotensin II type 1 receptor agonistic autoantibodies (AT<sub>1</sub>‐AAs) mediate the increased release of soluble endoglin (sEng) in women with preeclampsia.</p> </sec> <sec id="aji12340-sec-0002" sec-type="section"> <title>Method of study</title> <p>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 AT<sub>1</sub>‐AAs on these cells following treatment with an AT<sub>1</sub> receptor antagonist (losartan).</p> </sec> <sec id="aji12340-sec-0003" sec-type="section"> <title>Results</title> <p>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.</p> </sec> <sec id="aji12340-sec-0004" sec-type="section"> <title>Conclusion</title> <p>AT<sub>1</sub>‐AAs may be related to the increased release of sEng observed during preeclampsia and may play important roles in the pathology of this disorder.</p> </sec> </abstract>