Evidence map›Paper›PMID 24966239›Full record

ArticleJournal of the Royal Society, Interface2014

Shear-induced force transmission in a multicomponent, multicell model of the endothelium.

Mahsa Dabagh, Payman Jalali, Peter J Butler, John M Tarbell

Abstract read
In one paragraph

Article in Journal of the Royal Society, Interface, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
–field-weighted citation impact
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

19 citing papers in PubMed.

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  19. Fluid shear, intercellular stress, and endothelial cell alignment.American journal of physiology. Cell physiology · 2015
    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

4 authors.

Mahsa DabaghSchool of Technology, Lappeenranta University of Technology, Lappeenranta, Finland mdabagh@lut.fi.
Payman JalaliSchool of Technology, Lappeenranta University of Technology, Lappeenranta, Finland.
Peter J ButlerDepartment of Biomedical Engineering, The Pennsylvania State University, Pennsylvania, PA, USA.
John M TarbellDepartment of Biomedical Engineering, The City College of New York, New York, USA.

Funding

The Endothelial Glycocalyx: Its Structure and Function and as a MechanotransducerR01HL094889 · NHLBI · CITY COLLEGE OF NEW YORK · PI TARBELL, JOHN M · 2010 to 2014
$2.4M
NHLBI NIH HHS HL94889
6 · The paper itself

Abstract

Haemodynamic forces applied at the apical surface of vascular endothelial cells (ECs) provide the mechanical signals at intracellular organelles and through the inter-connected cellular network. The objective of this study is to quantify the intracellular and intercellular stresses in a confluent vascular EC monolayer. A novel three-dimensional, multiscale and multicomponent model of focally adhered ECs is developed to account for the role of potential mechanosensors (glycocalyx layer, actin cortical layer, nucleus, cytoskeleton, focal adhesions (FAs) and adherens junctions (ADJs)) in mechanotransmission and EC deformation. The overriding issue addressed is the stress amplification in these regions, which may play a role in subcellular localization of mechanotransmission. The model predicts that the stresses are amplified 250-600-fold over apical values at ADJs and 175-200-fold at FAs for ECs exposed to a mean shear stress of 10 dyne cm(-2). Estimates of forces per molecule in the cell attachment points to the external cellular matrix and cell-cell adhesion points are of the order of 8 pN at FAs and as high as 3 pN at ADJs, suggesting that direct force-induced mechanotransmission by single molecules is possible in both. The maximum deformation of an EC in the monolayer is calculated as 400 nm in response to a mean shear stress of 1 Pa applied over the EC surface which is in accord with measurements. The model also predicts that the magnitude of the cell-cell junction inclination angle is independent of the cytoskeleton and glycocalyx. The inclination angle of the cell-cell junction is calculated to be 6.6° in an EC monolayer, which is somewhat below the measured value (9.9°) reported previously for ECs subjected to 1.6 Pa shear stress for 30 min. The present model is able, for the first time, to cross the boundaries between different length scales in order to provide a global view of potential locations of mechanotransmission.

Indexed as

Shear StrengthActinsAdherens JunctionsCell AdhesionCytoskeletonEndothelial CellsFinite Element AnalysisFocal AdhesionsGlycocalyxHemodynamicsHumansHuman Umbilical Vein Endothelial CellsMechanotransduction, CellularModels, TheoreticalSoftwareStress, MechanicalActinsadherens junctionsendothelial cell mechanicsfocal adhesionsglycocalyxmechanotransmissionstress fibres

Identifiers

PMID24966239
PMCPMC4233691

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.