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

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...

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Autores principales:	Tina Cronqvist, Dionne Tannetta, Matthias Mörgelin, Mattias Belting, Ian Sargent, Mary Familari, Stefan R. Hansson
Formato:	article
Lenguaje:	EN
Publicado:	Nature Portfolio 2017
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/b7b849aaf5b4494c8909359f5008ddf0
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spelling	oai:doaj.org-article:b7b849aaf5b4494c8909359f5008ddf02021-12-02T15:06:01ZSyncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells10.1038/s41598-017-04468-02045-2322https://doaj.org/article/b7b849aaf5b4494c8909359f5008ddf02017-07-01T00:00:00Zhttps://doi.org/10.1038/s41598-017-04468-0https://doaj.org/toc/2045-2322Abstract 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.Tina CronqvistDionne TannettaMatthias MörgelinMattias BeltingIan SargentMary FamilariStefan R. HanssonNature PortfolioarticleMedicineRScienceQENScientific Reports, Vol 7, Iss 1, Pp 1-14 (2017)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Tina Cronqvist Dionne Tannetta Matthias Mörgelin Mattias Belting Ian Sargent Mary Familari Stefan R. Hansson Syncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells
description	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.
format	article
author	Tina Cronqvist Dionne Tannetta Matthias Mörgelin Mattias Belting Ian Sargent Mary Familari Stefan R. Hansson
author_facet	Tina Cronqvist Dionne Tannetta Matthias Mörgelin Mattias Belting Ian Sargent Mary Familari Stefan R. Hansson
author_sort	Tina Cronqvist
title	Syncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells
title_short	Syncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells
title_full	Syncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells
title_fullStr	Syncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells
title_full_unstemmed	Syncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells
title_sort	syncytiotrophoblast derived extracellular vesicles transfer functional placental mirnas to primary human endothelial cells
publisher	Nature Portfolio
publishDate	2017
url	https://doaj.org/article/b7b849aaf5b4494c8909359f5008ddf0
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Syncytiotrophoblast derived extracellular vesicles transfer functional placental miRNAs to primary human endothelial cells

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