Evidence map›Paper›PMID 28624707›Full record

ArticleBiomaterials2017

Substrate stiffness and VE-cadherin mechano-transduction coordinate to regulate endothelial monolayer integrity.

Roberto C Andresen Eguiluz, Kerim B Kaylan, Gregory H Underhill, Deborah E Leckband

Open access · greenAbstract read
In one paragraph

Article in Biomaterials, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed
4.2field-weighted citation impact, top 5% 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

48 citing papers in PubMed, 95 citations in OpenAlex.

  1. Article
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  7. Beyond classical collagen: basement membrane collagen IV in age-associated lung diseases.European respiratory review : an official journal of the European Respiratory Society · 2025
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  12. Notch transcriptional target tmtc1 maintains vascular homeostasis.Cellular and molecular life sciences : CMLS · 2024
    Article
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  15. Review
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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

4 authors at 1 institution in 1 country.

Roberto C Andresen EguiluzDepartment of Chemical and Biomolecular Engineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801, United States.
Kerim B KaylanDepartment of Bioengineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801, United States.
Gregory H UnderhillDepartment of Bioengineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801, United States.
Deborah E LeckbandDepartment of Chemical and Biomolecular Engineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801, United States; Department of Bioengineering, University of Illinois at Urbana-Champaign, Urbana, IL 61801, United States; Carl R. Woese Institute for Genomic Biology, University of Illinois at Urbana-Champaign, Urbana, IL 61801, United States. Electronic address: leckband@illinois.edu.
University of Illinois Urbana-Champaign · US

Funding

TRPC6 Regulation of Lung Endothelial Barrier FunctionP01HL060678 · NHLBI · UNIVERSITY OF ILLINOIS AT CHICAGO · PI MALIK, ASRAR B. · 2000 to 2020
$40.1M
NHLBI NIH HHS P01 HL060678
6 · The paper itself

Abstract

The vascular endothelium is subject to diverse mechanical cues that regulate vascular endothelial barrier function. In addition to rigidity sensing through integrin adhesions, mechanical perturbations such as changes in fluid shear stress can also activate force transduction signals at intercellular junctions. This study investigated how extracellular matrix rigidity and intercellular force transduction, activated by vascular endothelial cadherin, coordinate to regulate the integrity of endothelial monolayers. Studies used complementary mechanical measurements of endothelial monolayers grown on patterned substrates of variable stiffness. Specifically perturbing VE-cadherin receptors activated intercellular force transduction signals that increased integrin-dependent cell contractility and disrupted cell-cell and cell-matrix adhesions. Further investigations of the impact of substrate rigidity on force transduction signaling demonstrated how cells integrate extracellular mechanics cues and intercellular force transduction signals, to regulate endothelial integrity and global tissue mechanics. VE-cadherin specific signaling increased focal adhesion remodeling and cell contractility, while sustaining the overall mechanical equilibrium at the mesoscale. Conversely, increased substrate rigidity exacerbates the disruptive effects of intercellular force transduction signals, by increasing heterogeneity in monolayer stress distributions. The results provide new insights into how substrate stiffness and intercellular force transduction coordinate to regulate endothelial monolayer integrity.

Indexed as

Mechanotransduction, CellularAntigens, CDBiocompatible MaterialsBiomechanical PhenomenaCadherin 5CadherinsCell AdhesionCell LineCell-Matrix JunctionsEndothelial CellsEndothelium, VascularFocal AdhesionsHumansHydrogelsIntercellular JunctionsStress, MechanicalAntigens, CDBiocompatible MaterialsCadherin 5CadherinsHydrogelsCell tractionMagnetic twisting cytometryMechanotransductionMicropatterned substratesVE-cadherin

Identifiers

PMID28624707
PMCPMC5757379
OpenAlexW2622340093

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.