Evidence map›Paper›PMID 25157233›Full record

ArticleFrontiers in pharmacology2014

Extravillous trophoblast cells-derived exosomes promote vascular smooth muscle cell migration.

Carlos Salomon, Sarah Yee, Katherin Scholz-Romero, Miharu Kobayashi, Kanchan Vaswani, David Kvaskoff, Sebastian E Illanes, Murray D Mitchell, Gregory E Rice

Abstract read
In one paragraph

Article in Frontiers in pharmacology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
–field-weighted citation impact
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

64 citing papers in PubMed.

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  16. A thermo-resistant and RNase-sensitive cargo fromJournal of extracellular biology · 2023
    Article
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4 more citing papers are in PubMed but not listed here.

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

9 authors.

Carlos SalomonCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia ; Department of Obstetric and Gynaecology, Faculty of Medicine, Universidad de los Andes Santiago, Chile.
Sarah YeeCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia.
Katherin Scholz-RomeroCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia.
Miharu KobayashiCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia.
Kanchan VaswaniCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia.
David KvaskoffCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia.
Sebastian E IllanesCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia ; Department of Obstetric and Gynaecology, Faculty of Medicine, Universidad de los Andes Santiago, Chile.
Murray D MitchellCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia.
Gregory E RiceCentre for Clinical Diagnostics, Royal Brisbane and Women's Hospital, University of Queensland Centre for Clinical Research Brisbane, QLD, Australia ; Department of Obstetric and Gynaecology, Faculty of Medicine, Universidad de los Andes Santiago, Chile.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundVascular smooth muscle cells (VSMCs) migration is a critical process during human uterine spiral artery (SpA) remodeling and a successful pregnancy. Extravillous trophoblast cells (EVT) interact with VSMC and enhance their migration, however, the mechanisms by which EVT remodel SpA remain to be fully elucidated. We hypothesize that exosomes released from EVT promote VSMC migration.

methodsJEG-3 and HTR-8/SVneo cell lines were used as models for EVT. Cells were cultured at 37°C and humidified under an atmosphere of 5% CO2-balanced N2 to obtain 8% O2. Cell-conditioned media were collected, and exosomes (exo-JEG-3 and exo- HTR-8/SVneo) isolated by differential and buoyant density centrifugation. The effects of exo-EVT on VSMC migration were established using a real-time, live-cell imaging system (Incucyte™). Exosomal proteins where identified by mass spectrometry and submitted to bioinformatic pathway analysis (Ingenuity software).

resultsHTR-8/SVneo cells were significantly more (~30%) invasive than JEG-3 cells. HTR-8/SVneo cells released 2.6-fold more exosomes (6.39 × 10(8) ± 2.5 × 10(8) particles/10(6) cells) compared to JEG-3 (2.86 × 10(8) ± 0.78 × 10(8) particles/10(6) cells). VSMC migration was significantly increased in the presence of exo-JEG-3 and exo-HTR-8/SVneo compared to control (-exosomes) (21.83 ± 0.49 h and 15.57 ± 0.32, respectively, vs. control 25.09 ± 0.58 h, p < 0.05). Sonication completely abolished the effect of exosomes on VSMC migration. Finally, mass spectrometry analysis identified unique exosomal proteins for each EVT cell line-derived exosomes.

conclusionThe data obtained in this study are consistent with the hypothesis that the release, content, and bioactivity of exosomes derived from EVT-like cell lines is cell origin-dependent and differentially regulates VSMC migration. Thus, an EVT exosomal signaling pathway may contribute to SpA remodeling by promoting the migration of VSMC out of the vessel walls.

Indexed as

cell migrationexosomesplacentapregnancyproteomics

Identifiers

PMID25157233
PMCPMC4128075

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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.