Decreased expression of apelin in placentas from severe pre-eclampsia patients. (November 2013)

• Record Type: Journal Article
• Authors: Inuzuka, Hiromi; Nishizawa, Haruki; Inagaki, Ayaka; Suzuki, Machiko; Ota, Sayuri; Miyamura, Hironori; Miyazaki, Jun; Sekiya, Takao; Kurahashi, Hiroki; Udagawa, Yasuhiro
• Is Part Of: Hypertension in pregnancy. Volume 32:Number 4(2013)
• Page Start: 410
• Page End: 421
• Publication Date: 2013-11
• Subjects: Hypertension in pregnancy -- Periodicals; Pregnancy -- Complications -- Periodicals; 618.3261
• DOI: 10.3109/10641955.2013.813535
• Languages: English
• ISSNs: 1064-1955

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <p> <italic>Objective</italic>: 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. <italic>Methods</italic>: 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. <italic>Results</italic>: Apelin messenger RNA is significantly decreased in pre-eclamptic placentas compared with normotensive pregnancies (<italic>p</italic> < 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. <italic>Conclusions</italic>: 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 <italic>via</italic> decreased angiogenic activity in placental implantation.</p> </abstract>