Abstract
We examined the effect of plasma incubation from preeclampsia pregnant on the antiangiogenic miR‐195‐5p expression. Higher miR‐195‐5p expression was found in cultures incubated with preeclampsia plasma compared to those incubated with healthy pregnant plasma. Next, as VEGF is a target of miR‐195‐5p we have quantified its expression by real‐time qPCR and ELISA. We found reduced VEGF levels in culture incubated with preeclampsia plasma. Therefore, we have concluded that the higher expression of miR‐195‐5p in endothelial cell cultures incubated with preeclampsia plasma may contribute to decreased expression of VEGFA (gene and protein) and increased antiangiogenic status in preeclampsia. Therefore, this miR may be an important target in preeclampsia.
Highlights
Introduction and objectiveDown-regulation of miR-195-5p has been associated with increased angiogenesis in human hepatocellular carcinoma [1]
Elevated miR-195-5p concentrations were found in placenta from pre-eclamptic compared to healthy pregnancy [3], and it is well known that pre-eclampsia is characterized by an anti-angiogenic status, including high levels of sFLT-1 and sEng, which contrast with low free vascular endothelial growth factor (VEGFA) concentrations [2, 4, 5]
We found increased miR-195 expression in human umbilical vascular endothelial cells (HUVECs) incubated with plasma from pre-eclamptic pregnant as compared those incubated with plasma from healthy pregnant (6.7-fold increase, and 2ÀDCq of 0.042 Æ 0.031 versus 0.008 Æ 0.003, respectively, P < 0.01; Fig. 1) HUVEC incubated with plasma from pre-eclamptic pregnant showed reduced VEGFA expression as compared to those incubated with plasma form healthy pregnant (À2.43-fold decrease, and 2ÀDCq of 0.005 Æ 0.004 versus 0.012 Æ 0.008 respectively, in preeclamptic versus healthy; P = 0.05, Fig. 1)
Summary
Introduction and objectiveDown-regulation of miR-195-5p has been associated with increased angiogenesis in human hepatocellular carcinoma [1]. Several studies have reported a relationship between maternal endothelial dysfunction and factors present in plasma/serum of pre-eclamptic pregnant [9,10,11] Those circulating factors are in part released by ischaemic placental tissue into maternal circulation, and target endothelial cells causing alterations in their function [8, 11]. Supporting this concept, endothelial cells incubated with plasma/serum from pre-eclamptic pregnant undergo in vitro modifications [10, 12], such as increased expression of the vasoconstrictor endothelin-1 [13, 14]
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