Decreased expression of apelin in placentas from severe pre-eclampsia patients

Decreased expression of apelin in placentas from severe pre-eclampsia patients
复制标题

DOI:
10.3109/10641955.2013.813535
复制
发表时间:
2013-01-01
影响因子:
1.5
通讯作者:
Udagawa, Yasuhiro
Udagawa, Yasuhiro
中科院分区:
医学4区
文献类型:
--
作者:
Inuzuka, Hiromi;Nishizawa, Haruki;Udagawa, Yasuhiro

文献摘要

被引文献

相似文献

目的:抗血管生成因子在子痫前期的发病中起重要作用。Apelin是一种小肽,可能潜在地充当血管生成因子。在本研究中,在RNA和蛋白质水平上检测了爱帕琳的表达。研究方法:我们使用定量逆转录聚合酶链反应、蛋白质印迹、酶联免疫吸附试验和免疫染色来比较先兆子痫患者和血压正常对照之间爱帕琳的表达。结果:子痫前期患者胎盘Apelin mRNA表达水平明显低于正常妊娠组(p < 0.05)。爱帕琳蛋白水平在先兆子痫胎盘中也低于对照,但在先兆子痫患者的母体循环中较高。Apelin及其受体APJ的免疫组织化学信号主要在绒毛膜绒毛中的合体滋养细胞和足月胎盘蜕膜中的滋养细胞系细胞的细胞质中检测到。在妊娠早期,在细胞膜上观察到更强的APJ信号。结论:apelin-APJ系统的功能性作用可能在妊娠早期,这增加了功能障碍的apelin-APJ系统通过胎盘植入中血管生成活性降低而导致先兆子痫发作的可能性。
Objective: It is well documented that anti-angiogenic factors are likely to play essential roles in the etiology of pre-eclampsia. Apelin is a small peptide that may potentially act as an angiogenic factor. The expression of apelin was examined at the RNA and protein levels in this study. Methods: We compared the expression of apelin, examined using quantitative reverse-transcription polymerase chain reaction, western blotting, enzyme-linked immunosorbent assay and immunostaining, between pre-eclamptic patients and normotensive controls. Results: Apelin messenger RNA is significantly decreased in pre-eclamptic placentas compared with normotensive pregnancies (p < 0.05). Apelin protein levels are also lower in pre-eclamptic placentas than the controls but higher in the maternal circulation in pre-eclampsia patients. Immunohistochemical signals for apelin and its receptor APJ were detected mainly in the cytoplasm of syncytiotrophoblasts in chorionic villi and trophoblast-lineage cells in the decidua of term placentas. In early gestation, stronger APJ signals were observed at the cellular membrane. Conclusions: A functional role of the apelin-APJ system is likely in early gestation, and this raises the possibility that a dysfunctional apelin-APJ system contributes to the onset of pre-eclampsia via decreased angiogenic activity in placental implantation.