Evidence map›Paper›PMID 31455807›Full record

ArticleScientific reports2019

Vimentin regulates Notch signaling strength and arterial remodeling in response to hemodynamic stress.

Nicole C A van Engeland, Freddy Suarez Rodriguez, Adolfo Rivero-Müller, Tommaso Ristori, Camille L Duran, Oscar M J A Stassen, Daniel Antfolk, Rob C H Driessen, Saku Ruohonen, Suvi T Ruohonen and 8 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed
6.4field-weighted citation impact, top 2% 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

50 citing papers in PubMed, 89 citations in OpenAlex.

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  15. Apoptotic Cell Death in Bicuspid-Aortic-Valve-Associated Aortopathy.International journal of molecular sciences · 2023
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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

18 authors at 5 institutions in 4 countries.

Nicole C A van EngelandÅbo Akademi University, Faculty of Science and Engineering, Biosciences, Turku, Finland.ORCID http://orcid.org/0000-0002-7883-3163
Freddy Suarez RodriguezÅbo Akademi University, Faculty of Science and Engineering, Biosciences, Turku, Finland.
Adolfo Rivero-MüllerÅbo Akademi University, Faculty of Science and Engineering, Biosciences, Turku, Finland.
Tommaso RistoriÅbo Akademi University, Faculty of Science and Engineering, Biosciences, Turku, Finland.
Camille L DuranDepartment of Molecular & Cellular Medicine, Texas A&M University Health Science Center, College Station, TX, 77843, Texas, USA.ORCID http://orcid.org/0000-0002-7614-3265
Oscar M J A StassenÅbo Akademi University, Faculty of Science and Engineering, Biosciences, Turku, Finland.ORCID http://orcid.org/0000-0001-7485-0903
Daniel AntfolkÅbo Akademi University, Faculty of Science and Engineering, Biosciences, Turku, Finland.
Rob C H DriessenEindhoven University of Technology, Department of Biomedical Engineering, 5600, MB, Eindhoven, The Netherlands.ORCID http://orcid.org/0000-0003-3660-9371
Saku RuohonenInstitute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland.
Suvi T RuohonenInstitute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland.
Salla NuutinenInstitute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland.
Eriika SavontausInstitute of Biomedicine, Research Centre for Integrative Physiology and Pharmacology, University of Turku, Turku, Finland.
Sandra LoerakkerEindhoven University of Technology, Department of Biomedical Engineering, 5600, MB, Eindhoven, The Netherlands.
Kayla J BaylessDepartment of Molecular & Cellular Medicine, Texas A&M University Health Science Center, College Station, TX, 77843, Texas, USA.
Marika SjöqvistÅbo Akademi University, Faculty of Science and Engineering, Biosciences, Turku, Finland.
Carlijn V C BoutenEindhoven University of Technology, Department of Biomedical Engineering, 5600, MB, Eindhoven, The Netherlands.
John E ErikssonTurku Bioscience, Åbo Akademi University and University of Turku, Turku, Finland.
Cecilia M SahlgrenÅbo Akademi University, Faculty of Science and Engineering, Biosciences, Turku, Finland. cecilia.sahlgren@abo.fi.
Åbo Akademi University · FIUniversity of Turku · FIEindhoven University of Technology · NLTexas A&M Health Science Center · USMedical University of Lublin · PL

Funding

Bronx-Einstein Training in Teaching and Research (BETTR), an IRACDA programK12GM102779 · NIGMS · ALBERT EINSTEIN COLLEGE OF MEDICINE, INC · PI Dianne Cox, Johanna Patricia Daily · 2012 to 2026
$9.2M
NIGMS NIH HHS K12 GM102779
6 · The paper itself

Abstract

The intermediate filament (IF) cytoskeleton has been proposed to regulate morphogenic processes by integrating the cell fate signaling machinery with mechanical cues. Signaling between endothelial cells (ECs) and vascular smooth muscle cells (VSMCs) through the Notch pathway regulates arterial remodeling in response to changes in blood flow. Here we show that the IF-protein vimentin regulates Notch signaling strength and arterial remodeling in response to hemodynamic forces. Vimentin is important for Notch transactivation by ECs and vimentin knockout mice (VimKO) display disrupted VSMC differentiation and adverse remodeling in aortic explants and in vivo. Shear stress increases Jagged1 levels and Notch activation in a vimentin-dependent manner. Shear stress induces phosphorylation of vimentin at serine 38 and phosphorylated vimentin interacts with Jagged1 and increases Notch activation potential. Reduced Jagged1-Notch transactivation strength disrupts lateral signal induction through the arterial wall leading to adverse remodeling. Taken together we demonstrate that vimentin forms a central part of a mechanochemical transduction pathway that regulates multilayer communication and structural homeostasis of the arterial wall.

Indexed as

HemodynamicsSignal TransductionStress, PhysiologicalVascular RemodelingAnimalsAortaHumansHuman Umbilical Vein Endothelial CellsJagged-1 ProteinMiceMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleReceptors, NotchTranscriptional ActivationVimentinJag1 protein, mouseJagged-1 ProteinReceptors, NotchVimentinVim protein, mouse

Identifiers

PMID31455807
PMCPMC6712036
OpenAlexW2970253393

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.