Evidence map›Paper›PMID 28676635›Full record

ArticleScientific reports2017

Syncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells.

Tina Cronqvist, Dionne Tannetta, Matthias Mörgelin, Mattias Belting, Ian Sargent, Mary Familari, Stefan R Hansson

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
8.6field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

53 citing papers in PubMed, 111 citations in OpenAlex.

  1. Article
  2. Review
  3. Frontiers in physiology · 2026
    Article
  4. Crosstalk of extracellular vesicles in maternal-fetal interaction.Frontiers in cell and developmental biology · 2026
    Review
  5. Article
  6. Review
  7. Article
  8. Review
  9. Article
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  11. Article
  12. Article
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  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Pre-eclampsia.Nature reviews. Disease primers · 2023
    Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Tina CronqvistLund University, Department of Clinical Sciences in Lund, Obstetrics and Gynecology, 22185, Lund, Sweden. tina.cronqvist@med.lu.se.ORCID 0000-0002-7401-1939
Dionne TannettaUniversity of Reading, Department of Food and Nutritional Sciences, Whiteknights, Reading, UK.
Matthias MörgelinLund University, Department of Clinical Sciences in Lund, Division of Infection Medicine, 22185, Lund, Sweden.
Mattias BeltingLund University, Department of Clinical Sciences, Lund, Oncology and Pathology, 22185, Lund, Sweden.
Ian SargentNuffield Department of Obstetrics and Gynaecology, John Radcliffe Hospital University of Oxford, OX3 9DU, Oxford, UK.
Mary FamilariSchool of Biosciences, University of Melbourne, Parkville, VIC, 3010, Australia.
Stefan R HanssonLund University, Department of Clinical Sciences in Lund, Obstetrics and Gynecology, 22185, Lund, Sweden.
Lund University · SEJohn Radcliffe Hospital · GBThe University of Melbourne · AUUniversity of Reading · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During the pregnancy associated syndrome preeclampsia (PE), there is increased release of placental syncytiotrophoblast extracellular vesicles (STBEVs) and free foetal haemoglobin (HbF) into the maternal circulation. In the present study we investigated the uptake of normal and PE STBEVs by primary human coronary artery endothelial cells (HCAEC) and the effects of free HbF on this uptake. Our results show internalization of STBEVs into primary HCAEC, and transfer of placenta specific miRNAs from STBEVs into the endoplasmic reticulum and mitochondria of these recipient cells. Further, the transferred miRNAs were functional, causing a down regulation of specific target genes, including the PE associated gene fms related tyrosine kinase 1 (FLT1). When co-treating normal STBEVs with HbF, the miRNA deposition is altered from the mitochondria to the ER and the cell membrane becomes ruffled, as was also seen with PE STBEVs. These findings suggest that STBEVs may cause endothelial damage and contribute to the endothelial dysfunction typical for PE. The miRNA mediated effects on gene expression may contribute to the oxidative and endoplasmic reticulum stress described in PE, as well as endothelial reprogramming that may underlay the increased risk of cardiovascular disease reported for women with PE later in life.

Indexed as

Biological TransportCell-Derived MicroparticlesCells, CulturedEndothelial CellsExtracellular VesiclesFemaleHumansMicroRNAsMicroscopy, ConfocalPlacentaPregnancyTrophoblastsMicroRNAs

Identifiers

PMID28676635
PMCPMC5496854
OpenAlexW2729813435

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.