Kobayashi Yusuke, Yamamoto Tatsuo, Chishima Fumihisa, Takahashi Hideki, Suzuki Manami
Department of Obstetrics and Gynecology, Nihon University School of Medicine, Tokyo, Japan.
Am J Reprod Immunol. 2015 Apr;73(4):285-91. doi: 10.1111/aji.12340. Epub 2014 Nov 7.
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.
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).
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.
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.
本研究调查了1型血管紧张素II受体激动性自身抗体（AT1 -AAs）是否介导子痫前期女性可溶性内皮糖蛋白（sEng）释放增加。
从正常妊娠或子痫前期女性中获取血清样本。用人早孕滋养层细胞与从这些血清中纯化的IgG进行培养，并测量上清液中sEng蛋白和mRNA表达水平。在用1型血管紧张素II受体拮抗剂（氯沙坦）处理后，我们还测定了AT1 -AAs对这些细胞的影响。
与从正常妊娠女性中分离的IgG相比，子痫前期患者的处理显著增加了滋养层细胞中sEng的产生和mRNA表达。氯沙坦联合处理显著减弱了滋养层细胞中sEng的释放和sEng mRNA表达。
AT1 -AAs可能与子痫前期期间观察到的sEng释放增加有关，并可能在该疾病的病理过程中起重要作用。
