Evidence map›Paper›PMID 37103858›Full record

ArticleMembranes2023

Endoplasmin Is a Hypoxia-Inducible Endoplasmic Reticulum-Derived Cargo of Extracellular Vesicles Released by Cardiac Cell Lines.

Anna Koncz, Lilla Turiák, Krisztina Németh, Dorina Lenzinger, Tünde Bárkai, Péter Lőrincz, Helga Zelenyánszki, Krisztina V Vukman, Edit I Buzás, Tamás Visnovitz

Open access · goldAbstract read
In one paragraph

Article in Membranes, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

14 citing papers in PubMed, 21 citations in OpenAlex.

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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

10 authors at 3 institutions in 1 country.

Anna KonczDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Üllői út 26, 1085 Budapest, Hungary.
Lilla TuriákResearch Centre for Natural Sciences, Institute of Organic Chemistry, Magyar Tudósok Körútja 2, 1117 Budapest, Hungary.ORCID 0000-0002-2139-8156
Krisztina NémethDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Üllői út 26, 1085 Budapest, Hungary.
Dorina LenzingerDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Üllői út 26, 1085 Budapest, Hungary.
Tünde BárkaiDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Üllői út 26, 1085 Budapest, Hungary.
Péter LőrinczDepartment of Anatomy, Cell and Developmental Biology, ELTE Eötvös Loránd University, Pázmány Péter sétány 1/c, 1117 Budapest, Hungary.
Helga ZelenyánszkiDepartment of Plant Physiology and Molecular Plant Biology, ELTE Eötvös Loránd University, Pázmány Péter sétány 1/c, 1117 Budapest, Hungary.
Krisztina V VukmanDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Üllői út 26, 1085 Budapest, Hungary.
Edit I BuzásDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Üllői út 26, 1085 Budapest, Hungary.ORCID 0000-0002-3744-206X
Tamás VisnovitzDepartment of Genetics, Cell and Immunobiology, Semmelweis University, Üllői út 26, 1085 Budapest, Hungary.
Semmelweis University · HUEötvös Loránd University · HUInstitute of Organic Chemistry · HU

Funding

Eötvös Loránd University Excellence Fund EKA 2022/045-P101ERA-NET Cofund, Horizon 2020 2019-2.1.7-ERA-NET-2021-00015Higher Education Excellence Program FIKPHungarian National Research, Development and Innovation Office (NFKIH) NVKP 16-1-2016-0004Hungarian Scientific Research Fund OTKA K120237Hungarian Scientific Research Fund OTKA KF138851Hungary Academy of Sciences LP2022-13/2022Innovation and Technology; Ministry for National Economy of Hungary VEKOP-2.3.2-16-2016-00002Innovation and Technology; Ministry for National Economy of Hungary VEKOP-2.3.3-15-2017-00016National Cardiovascular Laboratory Program RRF-2.3.1-21-2022-00003Semmelweis Innovation Fund STIA 2020-KFITherapeutic Thematic Program TKP2020-NKA-26
6 · The paper itself

Abstract

Cardiomyopathies are leading causes of human mortality. Recent data indicate that the cardiomyocyte-derived extracellular vesicles (EVs) released upon cardiac injury are present in circulation. This paper aimed to analyze EVs released under normal and hypoxic conditions by H9c2 (rat), AC16 (human) and HL1 (mouse) cardiac cell lines. Small (sEVs), medium (mEVs) and large EVs (lEVs) were separated from a conditioned medium by a combination of gravity filtration, differential centrifugation and tangential flow filtration. The EVs were characterized by microBCA, SPV lipid assay, nanoparticle tracking analysis, transmission and immunogold electron microscopy, flow cytometry and Western blotting. Proteomic profiles of the EVs were determined. Surprisingly, an endoplasmic reticulum chaperone, endoplasmin (ENPL, grp94 or gp96), was identified in the EV samples, and its association with EVs was validated. The secretion and uptake of ENPL was followed by confocal microscopy using GFP-ENPL fusion protein expressing HL1 cells. We identified ENPL as an internal cargo of cardiomyocyte-derived mEVs and sEVs. Based on our proteomic analysis, its presence in EVs was linked to hypoxia in HL1 and H9c2 cells, and we hypothesize that EV-associated ENPL may have a cardioprotective role by reducing cardiomyocyte ER stress.

Indexed as

cardiomyocyteendoplasmic reticulum stressexosomeextracellular vesiclemedium EVsmall EV

Identifiers

PMID37103858
PMCPMC10142439
OpenAlexW4365514120

What OpenQuestion holds

Textmetadata
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.