Evidence map›Paper›PMID 28158679›Full record

ArticleCardiovascular research2017

New insights into shear stress-induced endothelial signalling and barrier function: cell-free fluid versus blood flow.

Sulei Xu, Xiang Li, Kyle Brian LaPenna, Stanley David Yokota, Sabine Huke, Pingnian He

Open access · bronzeAbstract readComparative Study
In one paragraph

Article in Cardiovascular research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
2.0field-weighted citation impact, top 13% 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

18 citing papers in PubMed, 25 citations in OpenAlex.

  1. Trial
  2. Review
  3. Pannexins in the vasculature.American journal of physiology. Heart and circulatory physiology · 2025
    Review
  4. Role of shear stress-induced red blood cell released ATP in atherosclerosis.American journal of physiology. Heart and circulatory physiology · 2025
    Article
  5. Article
  6. Article
  7. Article
  8. Review
  9. Heterogeneous ATP patterns in microvascular networks.Journal of the Royal Society, Interface · 2023
    Article
  10. Review
  11. Article
  12. Article
  13. Article
  14. Observational
  15. Review
  16. Article
  17. Review
  18. 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

6 authors at 3 institutions in 1 country.

Sulei XuDepartment of Cellular and Molecular Physiology, College of Medicine, Pennsylvania University, 500 University Drive, Hershey, PA 17033, USA.
Xiang LiDepartment of Cellular and Molecular Physiology, College of Medicine, Pennsylvania University, 500 University Drive, Hershey, PA 17033, USA.
Kyle Brian LaPennaDepartment of Cellular and Molecular Physiology, College of Medicine, Pennsylvania University, 500 University Drive, Hershey, PA 17033, USA.
Stanley David YokotaDepartment of Physiology and Pharmacology, School of Medicine, West Virginia University, One Medical Center Drive, Morgantown, WV 26506, USA.
Sabine HukeDepartment of Medicine, University of Alabama at Birmingham, 901 19th street South. Birmingham, AL 35294, USA.
Pingnian HeDepartment of Cellular and Molecular Physiology, College of Medicine, Pennsylvania University, 500 University Drive, Hershey, PA 17033, USA.
Hershey (United States) · USUniversity of Alabama at Birmingham · USWest Virginia University · US

Funding

CELLULAR MODULATION OF MICROVESSEL PERMEABILITY IN VIVOR01HL056237 · NHLBI · WEST VIRGINIA UNIVERSITY · PI HE, PINGNIAN · 2001 to 2013
$3.1M
Nitric oxide and microvessel permeability in vivoR01HL130363 · NHLBI · PENNSYLVANIA STATE UNIV HERSHEY MED CTR · PI HE, PINGNIAN · 2017 to 2020
$1.9M
Nitric Oxide and Microvessel Permeability In VivoR01HL084338 · NHLBI · WEST VIRGINIA UNIVERSITY · PI HE, PINGNIAN · 2007 to 2011
$1.6M
Cardiomyocyte-mediated mechanisms of ischemiaR01HL128563 · NHLBI · VANDERBILT UNIVERSITY · PI PRABHU, SUMANTH D · 2015 to 2018
$1.5M
Microparticles and microvascular dysfunction in diabetesR01DK097391 · NIDDK · WEST VIRGINIA UNIVERSITY · PI HE, PINGNIAN · 2013 to 2016
$1.4M
CELLULAR MODULATION OF MICROVESSEL PERMEABILITY IN VIVOR29HL056237 · NHLBI · UNIVERSITY OF CALIFORNIA DAVIS · PI HE, PINGNIAN · 1997 to 2001
$121k
NHLBI NIH HHS R01 HL056237NHLBI NIH HHS R01 HL084338NHLBI NIH HHS R01 HL128563NHLBI NIH HHS R01 HL130363NHLBI NIH HHS R29 HL056237NIDDK NIH HHS R01 DK097391
6 · The paper itself

Abstract

aimsFluid shear stress (SS) is known to regulate endothelial cell (EC) function. Most of the studies, however, focused on the effects of cell-free fluid-generated wall SS on ECs. The objective of this study was to investigate how changes in blood flow altered EC signalling and endothelial function directly through wall SS and indirectly through SS effects on red blood cells (RBCs). METHODS AND

resultsExperiments were conducted in individually perfused rat venules. We experimentally induced changes in SS that were quantified by measured flow velocity and fluid viscosity. The concomitant changes in EC [Ca2+]i and nitric oxide (NO) were measured with fluorescent markers, and EC barrier function was assessed by fluorescent microsphere accumulation at EC junctions using confocal imaging. EC eNOS activation was evaluated by immunostaining. In response to changes in SS, increases in EC [Ca2+]i and gap formation occurred only in blood or RBC solution perfused vessels, whereas SS-dependent NO production and eNOS-Ser1177 phosphorylation occurred in both plasma and blood perfused vessels. A bioluminescent assay detected SS-dependent ATP release from RBCs. Pharmacological inhibition and genetic modification of pannexin-1 channels on RBCs abolished SS-dependent ATP release and SS-induced increases in EC [Ca2+]i and gap formation.

conclusionsSS-induced EC NO production occurs in both cell free fluid and blood perfused vessels, whereas SS-induced increases in EC [Ca2+]i and EC gap formation require the presence of RBCs, attributing to SS-induced pannexin-1 channel dependent release of ATP from RBCs. Thus, changes in blood flow alter vascular EC function through both wall SS and SS exerted on RBCs, and RBC released ATP contributes to SS-induced changes in EC barrier function.

Indexed as

Capillary PermeabilityMechanotransduction, CellularAdenosine TriphosphateAnimalsBlood Flow VelocityBlood ViscosityCalciumEndothelial CellsEnzyme ActivationErythrocytesFemaleGap JunctionsIn Vitro TechniquesNitric OxideNitric Oxide Synthase Type IIIPerfusionAdenosine TriphosphateCalciumNitric OxideNitric Oxide Synthase Type IIINos3 protein, ratATPEndothelial calciumMicrovessel permeabilityNitric oxideShear stress

Identifiers

PMID28158679
PMCPMC5852521
OpenAlexW2594421750

What OpenQuestion holds

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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.