Autoantibodies Isolated from Patients with Preeclampsia Induce Soluble Endoglin Production from Trophoblast Cells Via Interactions with Angiotensin II Type 1 Receptor.

Autoantibodies Isolated from Patients with Preeclampsia Induce Soluble Endoglin Production from Trophoblast Cells Via Interactions with Angiotensin II Type 1 Receptor.
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从先兆子痫患者中分离出的自身抗体通过与血管紧张素 II 1 型受体相互作用,诱导滋养层细胞产生可溶性内皮糖蛋白。

DOI:
10.1111/aji.12340
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发表时间:
2015
期刊:
Am J Reprod Immunol.
影响因子:
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通讯作者:
Suzuki M. Autoantibodies Isolated from Patients with Preeclampsia Induce Soluble Endoglin Production from Trophoblast Cells Via Interactions with Angiotensin II Type 1 Receptor.
Suzuki M. Autoantibodies Isolated from Patients with Preeclampsia Induce Soluble Endoglin Production from Trophoblast Cells Via Interactions with Angiotensin II Type 1 Receptor.
中科院分区:
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文献类型:
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作者:
Kobayashi Y;Yamamoto T;Chishima F;Takahashi H;Suzuki M. Autoantibodies Isolated from Patients with Preeclampsia Induce Soluble Endoglin Production from Trophoblast Cells Via Interactions with Angiotensin II Type 1 Receptor.

文献摘要

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问题本研究探讨了血管紧张素II 1型受体激动性自身抗体(AT 1-AA)是否介导先兆子痫女性可溶性内皮素(sEng)释放的增加。研究方法血清样本取自正常妊娠或先兆子痫女性。将人早孕期滋养层细胞与来源于这些血清的纯化IgG一起培养,并测量上清液中的sEng蛋白和mRNA表达水平。我们还确定了AT 1-AAs对这些细胞治疗后的AT 1受体拮抗剂(losartan)的影响。结果与正常妊娠的妇女分离的IgG相比,先兆子痫患者的治疗显着增加sEng生产和滋养层细胞mRNA的表达。结论AT 1-AAs可能与子痫前期sEng的释放增加有关,可能在子痫前期的发病机制中起重要作用。
ProblemThis 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 studySerum 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 AT1receptor antagonist (losartan).ResultsCompared 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.ConclusionAT1‐AAs may be related to the increased release of sEng observed during preeclampsia and may play important roles in the pathology of this disorder.