Evidence map›Paper›PMID 21775480›Full record

ArticleAmerican journal of physiology. Renal physiology2011

Acute laminar shear stress reversibly increases human glomerular endothelial cell permeability via activation of endothelial nitric oxide synthase.

Heather S Bevan, Sadie C Slater, Hayley Clarke, Paul A Cahill, Peter W Mathieson, Gavin I Welsh, Simon C Satchell

Open access · greenAbstract read
In one paragraph

Article in American journal of physiology. Renal physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 32 citations in OpenAlex.

  1. Review
  2. Article
  3. TRIM27 contributes to glomerular endothelial cell injury in lupus nephritis by mediating the FoxO1 signaling pathway.Laboratory investigation; a journal of technical methods and pathology · 2021
    Article
  4. Article
  5. Article
  6. Review
  7. Article
  8. Review
  9. Shear stress is normalized in glomerular capillaries following ⅚ nephrectomy.American journal of physiology. Renal physiology · 2015
    Article
  10. The effect of oscillatory mechanical stimulation on osteoblast attachment and proliferation.Materials science & engineering. C, Materials for biological applications · 2015
    Article
  11. Article
  12. Article
  13. 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

7 authors at 3 institutions in 2 countries.

Heather S BevanAcademic Renal Unit, University of Bristol, Southmead Hospital, Bristol, United Kingdom.
Sadie C Slater
Hayley Clarke
Paul A Cahill
Peter W Mathieson
Gavin I Welsh
Simon C Satchell
Southmead Hospital · GBUniversity of Bristol · GBDublin City University · IE

Funding

Biotechnology and Biological Sciences Research Council BB/G012776/1Medical Research Council G0800200Wellcome Trust 075731
6 · The paper itself

Abstract

Laminar shear stress is a key determinant of systemic vascular behavior, including through activation of endothelial nitric oxide synthase (eNOS), but little is known of its role in the glomerulus. We confirmed eNOS expression by glomerular endothelial cells (GEnC) in tissue sections and examined effects of acute exposure (up to 24 h) to physiologically relevant levels of laminar shear stress (10-20 dyn/cm(2)) in conditionally immortalized human GEnC. Laminar shear stress caused an orientation of GEnC and stress fibers parallel to the direction of flow and induced Akt and eNOS phosphorylation along with NO production. Inhibition of the phophatidylinositol (PI)3-kinase/Akt pathway attenuated laminar shear stress-induced eNOS phosphorylation and NO production. Laminar shear stress of 10 dyn/cm(2) had a dramatic effect on GEnC permeability, reversibly decreasing the electrical resistance across GEnC monolayers. Finally, the laminar shear stress-induced reduction in electrical resistance was attenuated by the NOS inhibitors l-N(G)-monomethyl arginine (l-NMMA) and l-N(G)-nitroarginine methyl ester (l-NAME) and also by inhibition of the PI3-kinase/Akt pathway. Hence we have shown for GEnC in vitro that acute permeability responses to laminar shear stress are dependent on NO, produced via activation of the PI3-kinase/Akt pathway and increased eNOS phosphorylation. These results suggest the importance of laminar shear stress and NO in regulating the contribution of GEnC to the permeability properties of the glomerular capillary wall.

Indexed as

Shear StrengthStress, MechanicalCapillary PermeabilityCells, CulturedElectric ImpedanceEndothelium, VascularEnzyme InhibitorsHumansKidney GlomerulusNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIomega-N-MethylargininePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-aktEnzyme InhibitorsNG-Nitroarginine Methyl EsterNitric Oxide Synthase Type IIIomega-N-MethylargininePhosphatidylinositol 3-KinasesPhosphoinositide-3 Kinase InhibitorsProto-Oncogene Proteins c-akt

Identifiers

PMID21775480
PMCPMC3191806
OpenAlexW1996722780

What OpenQuestion holds

Textmetadata
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.