Evidence map›Paper›PMID 32944194›Full record

ArticleJournal of extracellular vesicles2020

Characterization of brain-derived extracellular vesicles reveals changes in cellular origin after stroke and enrichment of the prion protein with a potential role in cellular uptake.

Santra Brenna, Hermann C Altmeppen, Behnam Mohammadi, Björn Rissiek, Florence Schlink, Peter Ludewig, Christoph Krisp, Hartmut Schlüter, Antonio Virgilio Failla, Carola Schneider and 3 more

Open access · goldAbstract read
In one paragraph

Article in Journal of extracellular vesicles, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.

0numbers the graph read from it
0cells of the map it votes in
69citing papers in PubMed
5.0field-weighted citation impact, top 3% 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

69 citing papers in PubMed, 116 citations in OpenAlex.

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  9. Increased circulating TREM2Brain, behavior, & immunity - health · 2026
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9 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

13 authors at 2 institutions in 1 country.

Santra BrennaNeurology Department, Experimental Research in Stroke and Inflammation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0001-8233-2110
Hermann C AltmeppenInstitute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0001-9439-6533
Behnam MohammadiInstitute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0002-9178-3949
Björn RissiekNeurology Department, Experimental Research in Stroke and Inflammation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0001-5327-5479
Florence SchlinkNeurology Department, Experimental Research in Stroke and Inflammation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Peter LudewigNeurology Department, Experimental Research in Stroke and Inflammation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0001-9025-6402
Christoph KrispInstitute of Clinical Chemistry and Laboratory Medicine, Mass Spectrometric Proteomics University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Hartmut SchlüterInstitute of Clinical Chemistry and Laboratory Medicine, Mass Spectrometric Proteomics University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0002-9358-7036
Antonio Virgilio FaillaUKE Microscopy Imaging Facility, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0002-7137-0506
Carola SchneiderHeinrich Pette Institute, Leibniz Institute for Experimental Virology, Hamburg, Germany.
Markus GlatzelInstitute of Neuropathology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0002-7720-8817
Berta PuigNeurology Department, Experimental Research in Stroke and Inflammation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0002-2255-8393
Tim MagnusNeurology Department, Experimental Research in Stroke and Inflammation, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.ORCID https://orcid.org/0000-0001-6232-9555
Universität Hamburg · DELeibniz Institute of Virology (LIV) · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Extracellular vesicles (EVs) are important means of intercellular communication and a potent tool for regenerative therapy. In ischaemic stroke, transient blockage of a brain artery leads to a lack of glucose and oxygen in the affected brain tissue, provoking neuronal death by necrosis in the core of the ischaemic region. The fate of neurons in the surrounding penumbra region depends on the stimuli, including EVs, received during the following hours. A detailed characterization of such stimuli is crucial not only for understanding stroke pathophysiology but also for new therapeutic interventions. In the present study, we characterize the EVs in mouse brain under physiological conditions and 24 h after induction of transient ischaemia in mice. We show that, in steady-state conditions, microglia are the main source of small EVs (sEVs), whereas after ischaemia the main sEV population originates from astrocytes. Brain sEVs presented high amounts of the prion protein (PrP), which were further increased after stroke. Moreover, EVs were enriched in a proteolytically truncated PrP fragment (PrP-C1). Because of similarities between PrP-C1 and certain viral surface proteins, we studied the cellular uptake of brain-derived sEVs from mice lacking (PrP-KO) or expressing PrP (WT). We show that PrP-KO-sEVs are taken up significantly faster and more efficiently than WT-EVs by primary neurons. Furthermore, microglia and astrocytes engulf PrP-KO-sEVs more readily than WT-sEVs. Our results provide novel information on the relative contribution of brain cell types to the sEV pool in murine brain and indicate that increased release of sEVs by astrocytes together with elevated levels of PrP in sEVs may play a role in intercellular communication at early stages after stroke. In addition, amounts of PrP (and probably PrP-C1) in brain sEVs seem to contribute to regulating their cellular uptake.

Indexed as

Astrocytesextracellular vesicles (EVs)ischaemiamicrogliaprion protein (PrP)proteolytic processingPrP-C1PrP knock-outstroke

Identifiers

PMID32944194
PMCPMC7480459
OpenAlexW3081919405

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

Registered trials

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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.