Evidence map›Paper›PMID 23102623›Full record

ArticleBiomaterials2013

The effect of substrate modulus on the growth and function of matrix-embedded endothelial cells.

Sylaja Murikipudi, Heiko Methe, Elazer R Edelman

Open access · bronzeAbstract read
In one paragraph

Article in Biomaterials, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.7field-weighted citation impact, top 18% 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

20 citing papers in PubMed, 60 citations in OpenAlex.

  1. Article
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  8. Review
  9. Stiffness Sensing by Cells.Physiological reviews · 2020
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Gelatinolytic activity of autocrine matrix metalloproteinase-9 leads to endothelial de-arrangement in Moyamoya disease.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2018
    Article
  15. Article
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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

3 authors at 2 institutions in 2 countries.

Sylaja MurikipudiHarvard-MIT Division of Health Sciences and Technology, Massachusetts Institute of Technology, Cambridge, MA 02139, USA. sylajam@mit.edu
Heiko Methe
Elazer R Edelman
Massachusetts Institute of Technology · USHarvard–MIT Division of Health Sciences and Technology · US

Funding

Vascular Drug Delivery - Supplement for EquipmentR01GM049039 · NIGMS · MASSACHUSETTS INSTITUTE OF TECHNOLOGY · PI EDELMAN, ELAZER R · 1994 to 2019
$8.9M
NIGMS NIH HHS R01 GM049039NIGMS NIH HHS R01 GM49039
6 · The paper itself

Abstract

Endothelial cells (EC) are potent bioregulatory cells, modulating thrombosis, inflammation and control over mural smooth muscle cells and vascular health. The biochemical roles of EC are retained when cells are embedded within three-dimensional (3D) denatured collagen matrices. Though substrate mechanics have long been known to affect cellular morphology and function and 3D-EC systems are increasingly used as therapeutic modalities little is known about the effect of substrate mechanics on EC in these 3D systems. In this work, we examined the effect of isolated changes in modulus on EC growth and morphology, extracellular matrix gene expression, modulation of smooth muscle cell growth, and immunogenicity. EC growth, but not morphology was dependent on scaffold modulus. Increased scaffold modulus reduced secretion of smooth muscle cell growth inhibiting heparan sulfate proteoglycans (HSPGs), but had no effect on secreted growth factors, resulting in a loss of smooth muscle cell growth inhibition by EC on high modulus scaffolds. Expression of ICAM-1, VCAM-1 and induction of CD4(+) T cell proliferation was reduced by increased scaffold modulus, and correlated with changes in integrin α5 expression. Expression of several common ECM proteins by EC on stiffer substrates dropped, including collagen IV(α1), collagen IV(α5), fibronectin, HSPGs (perlecan and biglycan). In contrast, expression of elastin and TIMPs were increased. This work shows even modest changes in substrate modulus can have a significant impact on EC function in three-dimensional systems. The mechanism of these changes is not clear, but the data presented here within suggests a model wherein EC attempt to neutralize changes in environmental force balance by altering ECM and integrin expression, leading to changes in effects on downstream signaling and function.

Indexed as

AortaCell LineCell ProliferationCells, CulturedCoculture TechniquesElastic ModulusEndothelial CellsExtracellular Matrix ProteinsGelatinGene ExpressionHeparan Sulfate ProteoglycansHumansIntegrinsIntercellular Adhesion Molecule-1Myocytes, Smooth MuscleTissue ScaffoldsExtracellular Matrix ProteinsGelatinHeparan Sulfate ProteoglycansIntegrinsIntercellular Adhesion Molecule-1Vascular Cell Adhesion Molecule-1

Identifiers

PMID23102623
PMCPMC3505450
OpenAlexW2065092812

What OpenQuestion holds

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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.