Evidence map›Paper›PMID 31600286›Full record

ArticlePloS one2019

eNOS-NO-induced small blood vessel relaxation requires EHD2-dependent caveolae stabilization.

Claudia Matthaeus, Xiaoming Lian, Séverine Kunz, Martin Lehmann, Cheng Zhong, Carola Bernert, Ines Lahmann, Dominik N Müller, Maik Gollasch, Oliver Daumke

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.1field-weighted citation impact, top 25% 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

12 citing papers in PubMed, 19 citations in OpenAlex.

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  12. Energy and Dynamics of Caveolae Trafficking.Frontiers in cell and developmental biology · 2020
    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

10 authors at 3 institutions in 1 country.

Claudia MatthaeusCrystallography, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.ORCID 0000-0003-3242-1195
Xiaoming LianCharité-Universitätsmedizin Berlin, Experimental and Clinical Research Center (ECRC), Campus Buch, Berlin, Germany.
Séverine KunzElectron Microscopy Core Facility, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Martin LehmannDepartment of Molecular Pharmacology & Cell Biology and Imaging Core Facility, Leibniz-Forschungsinstitut für Molekulare Pharmakologie, Berlin, Germany.
Cheng ZhongCharité-Universitätsmedizin Berlin, Experimental and Clinical Research Center (ECRC), Campus Buch, Berlin, Germany.
Carola BernertCrystallography, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Ines LahmannSignal Transduction/Developmental Biology, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Dominik N MüllerExperimental & Clinical Research Center, a cooperation between Charité Universitätsmedizin Berlin and Max Delbrück Center for Molecular Medicine, Berlin, Germany.
Maik GollaschCharité-Universitätsmedizin Berlin, Experimental and Clinical Research Center (ECRC), Campus Buch, Berlin, Germany.
Oliver DaumkeCrystallography, Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.
Max Delbrück Center · DECharité - Universitätsmedizin Berlin · DELeibniz-Forschungsinstitut für Molekulare Pharmakologie · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Endothelial nitric oxide synthase (eNOS)-related vessel relaxation is a highly coordinated process that regulates blood flow and pressure and is dependent on caveolae. Here, we investigated the role of caveolar plasma membrane stabilization by the dynamin-related ATPase EHD2 on eNOS-nitric oxide (NO)-dependent vessel relaxation. Loss of EHD2 in small arteries led to increased numbers of caveolae that were detached from the plasma membrane. Concomitantly, impaired relaxation of mesenteric arteries and reduced running wheel activity were observed in EHD2 knockout mice. EHD2 deletion or knockdown led to decreased production of nitric oxide (NO) although eNOS expression levels were not changed. Super-resolution imaging revealed that eNOS was redistributed from the plasma membrane to internalized detached caveolae in EHD2-lacking tissue or cells. Following an ATP stimulus, reduced cytosolic Ca2+ peaks were recorded in human umbilical vein endothelial cells (HUVECs) lacking EHD2. Our data suggest that EHD2-controlled caveolar dynamics orchestrates the activity and regulation of eNOS/NO and Ca2+ channel localization at the plasma membrane.

Indexed as

AnimalsBlood VesselsCalciumCarrier ProteinsCaveolaeCell MembraneCytosolHumansHuman Umbilical Vein Endothelial CellsMesenteric ArteriesMice, Inbred C57BLNitric OxideNitric Oxide Synthase Type IIIPhysical Conditioning, AnimalVasodilationCalciumCarrier ProteinsEHD2 protein, humanEHD2 protein, mouseNitric OxideNitric Oxide Synthase Type III

Identifiers

PMID31600286
PMCPMC6786623
OpenAlexW2979448042

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.