Elevated microRNA-520g in pre-eclampsia inhibits migration and invasion of trophoblasts

Jiang, Liansheng; Long, Anxiong; Longyi, Tan; Mei, Hong; Wu, Jingjing; Cai, Leiming; Li, Qian

doi:10.1016/j.placenta.2017.02.001

Cited by 50 publications

(30 citation statements)

References 26 publications

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“…Early diagnosis would enable closer monitoring and treatment of this condition, and may open the window for earlier intervention that might help reduce the associated risks to the fetus and the mother. In addition to investigations studying circulating free proteins and microRNAs for their biomarker potential, plasma extracellular vesicles, including exosomes, have been extensively studied in many medical fields for their diagnostic potential [38][39][40][41][42][43][44][45][46][47][48][49][50] .…”

Section: Discussionmentioning

confidence: 99%

Syncytiotrophoblast extracellular microvesicle profiles in maternal circulation for noninvasive diagnosis of preeclampsia

Levine

Habertheuer

Ram

et al. 2020

Sci Rep

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Preeclampsia is the most common placental pathology in pregnant females, with increased morbidity and mortality incurred on the mother and the fetus. There is a need for improved biomarkers for diagnosis and monitoring of this condition. Placental syncytiotrophoblasts at the maternal-fetal interface release nanoparticles, including extracellular microvesicles, into the maternal blood during pregnancy. Syncytiotrophoblast extracellular microvesicles (STEVs) are being studied for their diagnostic potential and for their potential physiologic role in preeclampsia. We hypothesized that STEV profiles in maternal circulation would be altered under conditions of preeclampsia compared to normal pregnancy. Extracellular vesicles (EVs) released by BeWo cells in vitro showed high expression of syncytin-1, but no plac1 expression, demonstrating that trophoblast cell EVs express syncytin-1 on their surface. Placental alkaline phosphatase also showed high expression on BeWo EVs, but due to concern for cross reactivity to highly prevalent isoforms of intestinal and bone alkaline phosphatase, we utilized syncytin-1 as a marker for STEVs. In vivo, syncytin-1 protein expression was confirmed in maternal plasma EVs from Control and Preeclampsia subjects by Western blot, and overall, lower expression was noted in samples from patients with preeclampsia (n = 8). By nanoparticle analysis, EV profiles from Control and Preeclampsia groups showed similar total plasma EV quantities (p = 0.313) and size distribution (p = 0.415), but STEV quantitative signal, marked by syncytin-1 specific EVs, was significantly decreased in the Preeclampsia group (p = 2.8 × 10 −11). Receiver operating characteristic curve demonstrated that STEV signal threshold cutoff of <0.316 was 95.2% sensitive and 95.6% specific for diagnosis of preeclampsia in this cohort (area under curve = 0.975 ± 0.020). In conclusion, we report that the syncytin-1 expressing EV profiles in maternal plasma might serve as a placental tissue specific biomarker for preeclampsia.

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Section: Discussionmentioning

confidence: 99%

Syncytiotrophoblast extracellular microvesicle profiles in maternal circulation for noninvasive diagnosis of preeclampsia

Levine

Habertheuer

Ram

et al. 2020

Sci Rep

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“…It is well established that the proliferation, migration and invasion of trophoblast cells into the pregnant uterus nourishes the developing fetus. Abnormal trophoblast invasion or migration may lead to the development of PE ( 18 , 26 ). The mechanisms of PE development are unclear and are thought to be multifactorial.…”

Section: Discussionmentioning

confidence: 99%

“…Accumulating evidence indicates that the abnormal miRNA expression contributes to PE development ( 16 , 17 ). For example, the upregulation of miR-520g can promote PE via the inhibition of trophoblast migration and invasion ( 18 ). The human placenta expresses numerous angiogenic factors that may be involved in maternal vascular adaptation to pregnancy, including vascular endothelial growth factor (VEGF).…”

Section: Introductionmentioning

confidence: 99%

miR‑203 contributes to pre‑eclampsia via inhibition of VEGFA expression

Liu

et al. 2018

Mol Med Report

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Pre-eclampsia (PE) is a common but complex condition that can occur in pregnancy. It is estimated to affect 3–8% of pregnancies worldwide. PE development is thought to be multifactorial and to involve the dysregulation of microRNA (miR) expression. However, the precise mechanisms of PE development remain unclear. The present study aimed to illustrate the association between miR-203 expression and PE development in samples of human placenta collected from mothers with (n=18) and without (n=20) PE. It was demonstrated that miR-203 expression was significantly increased in the PE placenta compared with the normal placenta samples, while the expression of vascular endothelial growth factor A (VEGFA) was decreased. In vitro experiments revealed that miR-203 overexpression significantly downregulated VEGFA expression and inhibited the proliferation, migration and invasion ability of HTR-8/SVneo cells. Suppression of miR-203 expression alleviated these effects. A luciferase reporter assay confirmed the interaction of the 3′-untranslated region of VEGFA with miR-203. Thus, miR-203 may have significant contribution to the development of PE by targeting VEGFA in the human placenta and may have potential as a biomarker or therapeutic target in the treatment of PE.

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“…In this context, miR-519d was proposed to play a pivotal role by targeting CXCL6, NR4A2, and FOXL2 transcripts (Xie et al, 2014; Xie and Sadovsky, 2016). The ectopic expression of additional C19MC-derived miRNAs also modulates migration and invasion of extra-villous trophoblasts, notably via the action of miR-519d-3p (Ding et al, 2015), miR-520g (Jiang et al, 2017), miR-517a/b (Anton et al, 2015) and miR-520c-3p (Takahashi et al, 2017). A role of C19MC in placenta metabolism, presumably in the adaptation to hypoxia, is also emerging.…”

Section: The Primate-specific Paternally-expressed C19mc Mirna Genesmentioning

confidence: 99%

Imprinted MicroRNA Gene Clusters in the Evolution, Development, and Functions of Mammalian Placenta

et al. 2019

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In mammals, the expression of a subset of microRNA (miRNA) genes is governed by genomic imprinting, an epigenetic mechanism that confers monoallelic expression in a parent-of-origin manner. Three evolutionarily distinct genomic intervals contain the vast majority of imprinted miRNA genes: the rodent-specific, paternally expressed C2MC located in intron 10 of the Sfmbt2 gene, the primate-specific, paternally expressed C19MC positioned at human Chr.19q13.4 and the eutherian-specific, maternally expressed miRNAs embedded within the imprinted Dlk1-Dio3 domains at human 14q32 (also named C14MC in humans). Interestingly, these imprinted miRNA genes form large clusters composed of many related gene copies that are co-expressed with a marked, or even exclusive, localization in the placenta. Here, we summarize our knowledge on the evolutionary, molecular, and physiological relevance of these epigenetically-regulated, recently-evolved miRNAs, by focusing on their roles in placentation and possibly also in pregnancy diseases (e.g., preeclampsia, intrauterine growth restriction, preterm birth).

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Elevated microRNA-520g in pre-eclampsia inhibits migration and invasion of trophoblasts

Cited by 50 publications

References 26 publications

Syncytiotrophoblast extracellular microvesicle profiles in maternal circulation for noninvasive diagnosis of preeclampsia

Syncytiotrophoblast extracellular microvesicle profiles in maternal circulation for noninvasive diagnosis of preeclampsia

miR‑203 contributes to pre‑eclampsia via inhibition of VEGFA expression

Imprinted MicroRNA Gene Clusters in the Evolution, Development, and Functions of Mammalian Placenta

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