Evidence map›Paper›PMID 34188159›Full record

ArticleScientific reports2021

High stretch induces endothelial dysfunction accompanied by oxidative stress and actin remodeling in human saphenous vein endothelial cells.

T Girão-Silva, M H Fonseca-Alaniz, J C Ribeiro-Silva, J Lee, N P Patil, L A Dallan, A B Baker, M C Harmsen, J E Krieger, A A Miyakawa

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
5.6field-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

20 citing papers in PubMed, 37 citations in OpenAlex.

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  13. Endothelial-Specific Targeting of RhoA Signaling via CD31 Antibody-Conjugated Nanoparticles.The Journal of pharmacology and experimental therapeutics · 2023
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  19. P- and E- selectin in venous thrombosis and non-venous pathologies.Journal of thrombosis and haemostasis : JTH · 2022
    Review
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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 3 countries.

T Girão-SilvaLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of Sao Paulo Medical School, Av. Dr. Eneas de Carvalho Aguiar, 44-Bloco II, 10 Andar, São Paulo, SP, 05403-000, Brazil.
M H Fonseca-AlanizLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of Sao Paulo Medical School, Av. Dr. Eneas de Carvalho Aguiar, 44-Bloco II, 10 Andar, São Paulo, SP, 05403-000, Brazil.
J C Ribeiro-SilvaLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of Sao Paulo Medical School, Av. Dr. Eneas de Carvalho Aguiar, 44-Bloco II, 10 Andar, São Paulo, SP, 05403-000, Brazil.
J LeeDepartment of Biomedical Engineering, Institute for Cellular and Molecular Biology, Institute for Biomaterials, Drug Delivery and Regenerative Medicine, Institute for Computational Engineering and Sciences, University of Texas at Austin, Austin, TX, USA.
N P PatilDepartment of Biomedical Engineering, Institute for Cellular and Molecular Biology, Institute for Biomaterials, Drug Delivery and Regenerative Medicine, Institute for Computational Engineering and Sciences, University of Texas at Austin, Austin, TX, USA.
L A DallanLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of Sao Paulo Medical School, Av. Dr. Eneas de Carvalho Aguiar, 44-Bloco II, 10 Andar, São Paulo, SP, 05403-000, Brazil.
A B BakerDepartment of Biomedical Engineering, Institute for Cellular and Molecular Biology, Institute for Biomaterials, Drug Delivery and Regenerative Medicine, Institute for Computational Engineering and Sciences, University of Texas at Austin, Austin, TX, USA.
M C HarmsenLaboratory for Cardiovascular Regenerative Medicine Research Group (CAVAREM), Department of Pathology and Medical Biology, University Medical Center Groningen, University of Groningen, Groningen, the Netherlands.
J E KriegerLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of Sao Paulo Medical School, Av. Dr. Eneas de Carvalho Aguiar, 44-Bloco II, 10 Andar, São Paulo, SP, 05403-000, Brazil. j.krieger@hc.fm.usp.br.
A A MiyakawaLaboratory of Genetics and Molecular Cardiology, Heart Institute (InCor), University of Sao Paulo Medical School, Av. Dr. Eneas de Carvalho Aguiar, 44-Bloco II, 10 Andar, São Paulo, SP, 05403-000, Brazil. ayumi.miyakawa@incor.usp.br.
Universidade de São Paulo · BRThe University of Texas at Austin · USUniversity of Groningen · NL

Funding

Mechanical Conditioning of Mesenchymal Stem Cells for Enhanced Recellularized Vascular GraftsR01HL141761 · NHLBI · UNIVERSITY OF TEXAS AT AUSTIN · PI BAKER, AARON BLAIR · 2018 to 2021
$1.6M
Syndecan-1 in Mechanosensing of Engineered MicroenvironmentsR21EB023551 · NIBIB · UNIVERSITY OF TEXAS AT AUSTIN · PI BAKER, AARON BLAIR · 2017 to 2018
$450k
Glycocalyx Mimetic Polysaccharides as Therapeutics for AtherosclerosisR21EB024147 · NIBIB · UNIVERSITY OF TEXAS AT AUSTIN · PI BAKER, AARON BLAIR · 2017 to 2018
$430k
NHLBI NIH HHS R01 HL141761NIBIB NIH HHS R21 EB023551NIBIB NIH HHS R21 EB024147NIH HHS 1R21EB023551-01NIH HHS 1R21EB024147-01A1
6 · The paper itself

Abstract

The rate of the remodeling of the arterialized saphenous vein conduit limits the outcomes of coronary artery bypass graft surgery (CABG), which may be influenced by endothelial dysfunction. We tested the hypothesis that high stretch (HS) induces human saphenous vein endothelial cell (hSVEC) dysfunction and examined candidate underlying mechanisms. Our results showed that in vitro HS reduces NO bioavailability, increases inflammatory adhesion molecule expression (E-selectin and VCAM1) and THP-1 cell adhesion. HS decreases F-actin in hSVECs, but not in human arterial endothelial cells, and is accompanied by G-actin and cofilin's nuclear shuttling and increased reactive oxidative species (ROS). Pre-treatment with the broad-acting antioxidant N-acetylcysteine (NAC) supported this observation and diminished stretch-induced actin remodeling and inflammatory adhesive molecule expression. Altogether, we provide evidence that increased oxidative stress and actin cytoskeleton remodeling play a role in HS-induced saphenous vein endothelial cell dysfunction, which may contribute to predisposing saphenous vein graft to failure.

Indexed as

Oxidative StressStress, MechanicalActinsEndothelial CellsHumansReactive Oxygen SpeciesSaphenous VeinTHP-1 CellsActinsReactive Oxygen Species

Identifiers

PMID34188159
PMCPMC8242094
OpenAlexW3173256907

What OpenQuestion holds

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LicenceCC BY
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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.