Expression of endothelial NO synthase, inducible NO synthase, and estrogen receptors alpha and beta in placental tissue of normal, preeclamptic, and intrauterine growth-restricted pregnancies
Expression of endothelial NO synthase, inducible NO synthase, and estrogen receptors alpha and beta in placental tissue of normal, preeclamptic, and intrauterine growth-restricted pregnancies
复制标题
DOI：
10.1369/jhc.4a6480.2005
复制
发表时间：
2005-12-01
影响因子：
3.2
通讯作者：
Jeschke, U
中科院分区：
文献类型：
--
作者：
Schiessl, B;Mylonas, I;Jeschke, U
在胎盘血液循环的生理学中，一氧化氮（NO）合酶似乎发挥着重要作用，尽管它们在病理胎盘中的表达及其作用仍不清楚。此外，NO合酶激活似乎与雌激素受体表达有关。因此，本研究的目的是调查子宫内生长受限（IUGR）胎盘、先兆子痫胎盘和正常健康对照胎盘中雌激素受体α（ERα）、雌激素受体β（ER）和内皮NO合酶（eNOS）和诱导型NO合酶（iNOS）的表达。诊断患者分娩后获得石蜡包埋的胎盘组织切片。使用半定量评分分析免疫组织化学反应的强度，并进行统计分析，以比较通过免疫组织化学和蛋白质印迹获得的eNOS、iNOS和ER β的表达在胎盘滋养层细胞中的表达。然而，与正常对照相比，先兆子痫胎盘的这些蛋白的表达强度显着升高。人类滋养层细胞的 eNOS、iNOS、ER α 和 ER β 表达不同，似乎导致 NO 输出降低和滋养层侵袭受损。我们的研究结果表明，所研究的蛋白表达减少与 IUGR 相关。
In the physiology of placental blood circulation, nitric oxide (NO) synthases seem to play important roles, although their expression in pathological placentas and their role is still unclear. In addition, NO synthase activation seems to be related to estrogen receptor expression. Therefore, the aims of this study were to investigate the expression of estrogen receptors alpha (ER alpha), estrogen receptor beta (ER and the endothelial NO synthase (eNOS), and inducible NO synthase (iNOS) in intrauterine growth-restricted (IUGR) placentas, preeclamptic placentas, and in normal healthy control placentas. Slides of paraffin-embedded placental tissue were obtained after delivery from patients diagnosed with IUGR, preeclampsia, and normal term placentas and analyzed for eNOS, iNOS as well as ER alpha and ER beta expression. Intensity of immunohistochemical reaction was analyzed using a semiquantitative score and statistical analysis was performed. In addition, Western blot experiments were performed for comparison of staining intensities obtained by immunohistochemistry and western blot. Expression of eNOS, iNOS, and ER beta is significantly reduced in trophoblast cells of placentas with IUGR. However, preeclamptic placentas demonstrated a significant elevated expression intensity of these proteins compared with normal controls. A different expression of eNOS, iNOS, ER alpha, and ER beta by human trophoblast cells seems to results in lower NO output and impaired trophoblast invasion. Results obtained in our study provide evidence that reduced expression of the investigated proteins is related to IUGR.