Evidence map›Paper›PMID 24583416›Full record

ArticleAtherosclerosis2014

Effect of shear stress on water and LDL transport through cultured endothelial cell monolayers.

Hongyan Kang, Limary M Cancel, John M Tarbell

Abstract read
In one paragraph

Article in Atherosclerosis, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

21 citing papers in PubMed, 36 citations in OpenAlex.

  1. Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026
    Review
  2. Review
  3. Article
  4. Article
  5. Article
  6. Pathophysiology of Atherosclerosis.International journal of molecular sciences · 2022
    Review
  7. Article
  8. Article
  9. Review
  10. Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Using cultured endothelial cells to study endothelial barrier dysfunction: Challenges and opportunities.American journal of physiology. Lung cellular and molecular physiology · 2016
    Review
  20. Article
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 2 institutions in 2 countries.

Hongyan KangKey Laboratory for Biomechanics and Mechanobiology of Ministry of Education, School of Biological Science and Medical Engineering, Beihang University, Beijing, China; Department of Biomedical Engineering, The City College of The City University of New York, New York, USA.
Limary M CancelDepartment of Biomedical Engineering, The City College of The City University of New York, New York, USA.
John M TarbellDepartment of Biomedical Engineering, The City College of The City University of New York, New York, USA. Electronic address: tarbell@ccny.cuny.edu.
City College of New York · USCity University of New York · US

Funding

SHEAR STRESS EFFECTS ON ENDOTHELIAL TRANSPORTR01HL057093 · NHLBI · PENNSYLVANIA STATE UNIVERSITY-UNIV PARK · PI TARBELL, JOHN M · 1997 to 2010
$2.7M
NHLBI NIH HHS HL57093NHLBI NIH HHS R01 HL057093
6 · The paper itself

Abstract

Previous animal experiments have shown that the transport of LDL into arterial walls is shear stress dependent. However, little work has probed shear effects on LDL transport in vitro where conditions are well defined and mechanisms are more easily explored. Therefore, we measured shear induced water and LDL fluxes across cultured bovine aortic endothelial (BAEC) monolayers in vitro and developed a three-pore model to describe the transport dynamics. Cell apoptosis was quantified by TdT-mediated dUTP nick end labeling (TUNEL) assay. We also examined the role of nitric oxide (NO) in shear induced water and LDL fluxes by incubating BAEC monolayers with an NO synthase inhibitor, NG-monomethyl-L-arginine (L-NMMA). Our results show that direct exposure of endothelial monolayers to 12 dyn/cm2 shear stress for 3 h elicited a 2.37-fold increase in water flux (Jv), a 3.00-fold increase in LDL permeability (Pe), a 1.32-fold increase in LDL uptake, and a 1.68-fold increase in apoptotic rate. L-NMMA treatment of BAEC monolayers blocked shear induced Jv response, but had no significant effect on shear responses of Pe and cell apoptosis. A long time shear exposure (12 h) of endothelial monolayers reduced Pe and apoptotic rate close to the baseline. These results suggest that an acute change in shear stress from a static baseline state induces increases in water flux that are mediated by an NO dependent mechanism. On the other hand, the permeability of endothelial monolayers to LDL is enhanced by a short term-shear application and reduced nearly to the baseline level by a longer time shear exposure, positively correlated to the leaky junctions forming around apoptotic cells.

Indexed as

RheologyStress, MechanicalAnimalsAntigens, CDAortaApoptosisBiological TransportCadherin 5CadherinsCattleCell Membrane PermeabilityCells, CulturedEndothelial CellsEndothelium, VascularLipoproteins, LDLModels, BiologicalAntigens, CDCadherin 5CadherinsLipoproteins, LDLNitric Oxideomega-N-MethylarginineWaterBovine aortic endothelial cellsLDL permeabilityLeaky junctionsShear stressWater flux

Identifiers

PMID24583416
PMCPMC3979984
OpenAlexW2034264424

What OpenQuestion holds

Textmetadata
LicenceTDM
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.