Evidence map›Paper›PMID 31048903›Full record

ArticlePLoS computational biology2019

Balance of mechanical forces drives endothelial gap formation and may facilitate cancer and immune-cell extravasation.

Jorge Escribano, Michelle B Chen, Emad Moeendarbary, Xuan Cao, Vivek Shenoy, Jose Manuel Garcia-Aznar, Roger D Kamm, Fabian Spill

Open access · goldAbstract read
In one paragraph

Article in PLoS computational biology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
4.5field-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

33 citing papers in PubMed, 76 citations in OpenAlex.

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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

8 authors at 5 institutions in 4 countries.

Jorge EscribanoDepartment of Mechanical Engineering, University of Zaragoza, Zaragoza, Spain.ORCID 0000-0001-8928-350X
Michelle B ChenDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.
Emad MoeendarbaryDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.
Xuan CaoDepartment of Materials Science and Engineering, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Vivek ShenoyDepartment of Materials Science and Engineering, University of Pennsylvania, Philadelphia, Pennsylvania, United States of America.
Jose Manuel Garcia-AznarDepartment of Mechanical Engineering, University of Zaragoza, Zaragoza, Spain.
Roger D KammDepartment of Biological Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.
Fabian SpillDepartment of Mechanical Engineering, Massachusetts Institute of Technology, Cambridge, Massachusetts, United States of America.ORCID 0000-0001-8462-5080
Massachusetts Institute of Technology · USUniversidad de Zaragoza · ESUniversity of Pennsylvania · USSingapore-MIT Alliance for Research and Technology · SGUniversity College London · GB

Funding

Research Supplement - Quantitative analyses of tumor cell extravasationU01CA202177 · NCI · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KAMM, ROGER D · 2015 to 2020
$4.2M
Modeling bi-directional signaling and cytoskeletal dynamics in 3D cell migrationsU01CA177799 · NCI · BOSTON UNIVERSITY (CHARLES RIVER CAMPUS) · PI GERTLER, FRANK B, KAMM, ROGER D · 2013 to 2017
$3.0M
Development of 3D vascularized model of Blood Brain Barrier and its application to Alzheimer disease researchR21NS105027 · NINDS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI KAMM, ROGER D · 2019 to 2020
$457k
Cancer Research UK 22057Cancer Research UK C416/A25145Cancer Research UK C57744/A22057NCI NIH HHS U01 CA177799NCI NIH HHS U01 CA202177NINDS NIH HHS R21 NS105027Wellcome Trust WT103883
6 · The paper itself

Abstract

The formation of gaps in the endothelium is a crucial process underlying both cancer and immune cell extravasation, contributing to the functioning of the immune system during infection, the unfavorable development of chronic inflammation and tumor metastasis. Here, we present a stochastic-mechanical multiscale model of an endothelial cell monolayer and show that the dynamic nature of the endothelium leads to spontaneous gap formation, even without intervention from the transmigrating cells. These gaps preferentially appear at the vertices between three endothelial cells, as opposed to the border between two cells. We quantify the frequency and lifetime of these gaps, and validate our predictions experimentally. Interestingly, we find experimentally that cancer cells also preferentially extravasate at vertices, even when they first arrest on borders. This suggests that extravasating cells, rather than initially signaling to the endothelium, might exploit the autonomously forming gaps in the endothelium to initiate transmigration.

Indexed as

Biomechanical PhenomenaCell AdhesionCell MovementEndothelial CellsEndothelium, VascularGap JunctionsHumansHuman Umbilical Vein Endothelial CellsNeoplasmsTransendothelial and Transepithelial Migration

Identifiers

PMID31048903
PMCPMC6497229
OpenAlexW2949955219

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.