Evidence map›Paper›PMID 26147292›Full record

ArticlePloS one2015

The Interaction between Fluid Wall Shear Stress and Solid Circumferential Strain Affects Endothelial Gene Expression.

Ronny Amaya, Alexis Pierides, John M Tarbell

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
6.5field-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

23 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Vascular endothelial integration of multiple biophysical stimuli.Frontiers in cardiovascular medicine · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. Article
  7. Role of blood flow in endothelial functionality: a review.Frontiers in cell and developmental biology · 2023
    Review
  8. Article
  9. Role of Vascular Smooth Muscle Cell Phenotype Switching in Arteriogenesis.International journal of molecular sciences · 2021
    Review
  10. Review
  11. Review
  12. Review
  13. Article
  14. Article
  15. Review
  16. Article
  17. Article
  18. Article
  19. Article
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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

3 authors at 1 institution in 1 country.

Ronny AmayaDepartment of Biomedical Engineering, City College of New York, City University of New York, New York, New York, 10031, United States of America.
Alexis PieridesDepartment of Biomedical Engineering, City College of New York, City University of New York, New York, New York, 10031, United States of America.
John M TarbellDepartment of Biomedical Engineering, City College of New York, City University of New York, New York, New York, 10031, United States of America.
City College of New York · US

Funding

Hemodynamic Forces Affect Endothelial Cell Pheotype in Arterial DiseaseR01HL086543 · NHLBI · CITY COLLEGE OF NEW YORK · PI TARBELL, JOHN M · 2008 to 2011
$1.5M
NHLBI NIH HHS HL 086543NHLBI NIH HHS R01 HL086543
6 · The paper itself

Abstract

Endothelial cells lining the walls of blood vessels are exposed simultaneously to wall shear stress (WSS) and circumferential stress (CS) that can be characterized by the temporal phase angle between WSS and CS (stress phase angle - SPA). Regions of the circulation with highly asynchronous hemodynamics (SPA close to -180°) such as coronary arteries are associated with the development of pathological conditions such as atherosclerosis and intimal hyperplasia whereas more synchronous regions (SPA closer to 0°) are spared of disease. The present study evaluates endothelial cell gene expression of 42 atherosclerosis-related genes under asynchronous hemodynamics (SPA=-180 °) and synchronous hemodynamics (SPA=0 °). This study used a novel bioreactor to investigate the cellular response of bovine aortic endothelial cells (BAECS) exposed to a combination of pulsatile WSS and CS at SPA=0 or SPA=-180. Using a PCR array of 42 genes, we determined that BAECS exposed to non-reversing sinusoidal WSS (10±10 dyne/cm2) and CS (4 ± 4%) over a 7 hour testing period displayed 17 genes that were up regulated by SPA = -180 °, most of them pro-atherogenic, including NFκB and other NFκB target genes. The up regulation of NFκB p50/p105 and p65 by SPA =-180° was confirmed by Western blots and immunofluorescence staining demonstrating the nuclear translocation of NFκB p50/p105 and p65. These data suggest that asynchronous hemodynamics (SPA=-180 °) can elicit proatherogenic responses in endothelial cells compared to synchronous hemodynamics without shear stress reversal, indicating that SPA may be an important parameter characterizing arterial susceptibility to disease.

Indexed as

AnimalsAortaAtherosclerosisCattleCells, CulturedCoronary VesselsEndothelial CellsEndothelium, VascularGene ExpressionHemodynamicsModels, CardiovascularNF-kappa BPulsatile FlowStress, MechanicalNF-kappa B

Identifiers

PMID26147292
PMCPMC4492743
OpenAlexW2281259307

What OpenQuestion holds

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LicenceCC BY
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.