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子痫前期妊娠胎盘和蜕膜组织中的类二十烷酸生物合成酶:血栓素 A2 合酶基因表达增加。

Eicosanoid biosynthetic enzymes in placental and decidual tissues from preeclamptic pregnancies: increased expression of thromboxane-A2 synthase gene.

作者信息

Woodworth S H, Li X, Lei Z M, Rao C V, Yussman M A, Spinnato J A, Yokoyama C, Tanabe T, Ullrich V

机构信息

Department of Obstetrics and Gynecology, University of Louisville School of Medicine, Kentucky 40292.

出版信息

J Clin Endocrinol Metab. 1994 May;78(5):1225-31. doi: 10.1210/jcem.78.5.8175982.

Abstract

Preeclampsia is a disease of late pregnancy characterized by hypertension, edema, and proteinuria, in which vasoconstriction, platelet aggregation, and reduced uteroplacental blood flow contribute to preterm delivery, perinatal morbidity, and mortality. Increased thromboxane-A2 (TXA2) and/or decreased prostacyclin (PGI2) have been implicated as causative factors of this disease. The present studies investigated the expression of TXA2 synthase gene along with those of TXA2 receptors, PGI2 synthase, cyclooxygenase-1 (COX-1), and COX-2 in placental and decidual tissue from preeclamptic and normal pregnancies. In situ hybridization and immunocytochemistry showed that primarily trophoblast layer and decidual cells express TXA2 synthase, COX-1, and COX-2 enzymes. Immunocytochemistry for PGI2 synthase and in situ hybridization for TXA2 receptors showed similar results. Trophoblast layer and decidua from preeclamptic pregnancies contained a greater abundance of mRNA and protein of TXA2 synthase than the matched normal pregnancies. In summary, our findings suggest that an increased local expression of TXA2 synthase could be responsible for local and/or peripheral vascular changes in preeclampsia.

摘要

子痫前期是一种妊娠晚期疾病,其特征为高血压、水肿和蛋白尿,其中血管收缩、血小板聚集以及子宫胎盘血流减少会导致早产、围产期发病率和死亡率。血栓素 - A2(TXA2)增加和/或前列环素(PGI2)减少被认为是该疾病的致病因素。本研究调查了子痫前期和正常妊娠的胎盘及蜕膜组织中TXA2合酶基因以及TXA2受体、PGI2合酶、环氧化酶 - 1(COX - 1)和环氧化酶 - 2(COX - 2)的表达。原位杂交和免疫细胞化学显示,主要是滋养层和蜕膜细胞表达TXA2合酶、COX - 1和COX - 2酶。PGI2合酶的免疫细胞化学和TXA2受体的原位杂交显示了相似的结果。子痫前期妊娠的滋养层和蜕膜中TXA2合酶的mRNA和蛋白质含量比匹配的正常妊娠更多。总之,我们的研究结果表明,TXA2合酶局部表达增加可能是子痫前期局部和/或外周血管变化的原因。

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