The Expression of Placental Proteoglycans in Pre-Eclampsia

Abstract

Background/Aims: Pre-eclampsia (PE) is one of the leading causes of maternal and perinatal morbidity and mortality. PE is defined clinically as the onset of maternal hypertension and proteinuria following 20 weeks of gestation. It is associated with altered maternal uterine decidual spiral artery remodelling, which may lead to reduced blood flow and increased thrombosis within the uteroplacental vasculature. Proteoglycans (PGs) are macromolecules which have (in combination with glycosaminoglycans) important anticoagulant roles in vascular endothelial environments, including the uteroplacental circulation. The hypothesis under consideration in this study was that differential expression of placental PGs may be associated with PE. Methods: PE and control placental samples were collected with ethics approval and patient consent. RNA and protein were extracted and real-time PCR and Western immunoblotting were performed to determine the expression of the PGs in the samples. Results: Of the nine PGs investigated, none showed increased expression, whereas the mRNA and protein expression of five of them was significantly decreased in the placentae of pre-eclamptic women compared to gestation-matched controls. Conclusion: Therefore, the results of this study support the hypothesis that a placental PG deficiency may contribute to the placental thrombotic lesions characteristic of PE.

Expression and Clinical Significance of ATP-Binding Cassette Transporter 1 in Serum and Placental Tissue in Chinese Patients with Preeclampsia

“…Furthermore, in another study using animal models, the plasma of ABCA1-knockout mice did not contain HDL, and the mice appeared to be atherosclerosis-sensitive [31]. Although selective ABCA1 gene deletion in macrophages did not considerably affect the plasma HDL concentration, it was associated with the pathogenesis of atherosclerosis to a certain extent [12]. In a study by Repa et al [32], an increase in ABCA1 not only enhanced the efflux of cholesterol from macrophages and improved the RCT, but also increased the secretion of cholesterol in the intestinal mucosa, resulting in decreased absorption of cholesterol.…”

“…The decline in either the expression or the activity of ABCA1 may alter the function of ABCA1, leading to a modification of serum lipid levels, thereby causing atherogenesis [12,13]. We investigated the role and clinical significance of ABCA1 in the pathogenesis of PE by measuring serum and placental ABCA1 expression and the blood lipid profile in pregnant women with PE, as well as the correlation between ABCA1 expression and blood lipid concentration.…”

Antiangiogenic effects of decorin restored by unfractionated, low molecular weight, and nonanticoagulant heparins

“…[20][21][22][23][24][25] In our previous work, we showed that the messenger RNA and protein expression of the proteoglycan decorin (DCN) was reduced in PE-and FGR-affected placentae compared with controls. [26][27][28] Furthermore, we also showed that downregulation of DCN in human microvascular endothelial cells resulted in decreased cell growth and proliferation, decreased network formation (angiogenesis), and a modest increase in thrombin generation. 26 We also demonstrated that DCN was downregulated in the first trimester in women who went on to develop growth-restricted infants, suggesting that there is both a temporal relationship and biologic plausibility for the association between reduced DCN expression and subsequent development of PE/FGR.…”

Expression of Biglycan in First Trimester Chorionic Villous Sampling Placental Samples and Altered Function in Telomerase-Immortalized Microvascular Endothelial Cells

“…In fact, the expression of BGN is decreased in placentae affected by FGR, 18 but not in PE. 53 Therefore, it is plausible that the decrease in CXCL12 we observed in this study is unique to the pathogenesis of FGR, either as a result of a multitude of changes contributing to the disease or simply by the reduction in BGN expression alone.…”