Evidence map›Paper›PMID 29610298›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2018

Mechanosensitivity of Jagged-Notch signaling can induce a switch-type behavior in vascular homeostasis.

Sandra Loerakker, Oscar M J A Stassen, Fleur M Ter Huurne, Marcelo Boareto, Carlijn V C Bouten, Cecilia M Sahlgren

Erratum issuedAbstract readComparative Study
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing 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

42 citing papers in PubMed.

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  6. YAP/TAZ drives Notch and angiogenesis mechanoregulation in silico.NPJ systems biology and applications · 2024
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

6 authors.

Sandra LoerakkerDepartment of Biomedical Engineering, Eindhoven University of Technology, 5600 MB Eindhoven, The Netherlands; s.loerakker@tue.nl c.m.sahlgren@tue.nl.ORCID 0000-0002-9574-1623
Oscar M J A StassenDepartment of Biomedical Engineering, Eindhoven University of Technology, 5600 MB Eindhoven, The Netherlands.
Fleur M Ter HuurneDepartment of Biomedical Engineering, Eindhoven University of Technology, 5600 MB Eindhoven, The Netherlands.
Marcelo BoaretoDepartment of Biosystems Science and Engineering, ETH Zurich, 4058 Basel, Switzerland.
Carlijn V C BoutenDepartment of Biomedical Engineering, Eindhoven University of Technology, 5600 MB Eindhoven, The Netherlands.ORCID 0000-0003-1035-5094
Cecilia M SahlgrenDepartment of Biomedical Engineering, Eindhoven University of Technology, 5600 MB Eindhoven, The Netherlands; s.loerakker@tue.nl c.m.sahlgren@tue.nl.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Hemodynamic forces and Notch signaling are both known as key regulators of arterial remodeling and homeostasis. However, how these two factors integrate in vascular morphogenesis and homeostasis is unclear. Here, we combined experiments and modeling to evaluate the impact of the integration of mechanics and Notch signaling on vascular homeostasis. Vascular smooth muscle cells (VSMCs) were cyclically stretched on flexible membranes, as quantified via video tracking, demonstrating that the expression of Jagged1, Notch3, and target genes was down-regulated with strain. The data were incorporated in a computational framework of Notch signaling in the vascular wall, where the mechanical load was defined by the vascular geometry and blood pressure. Upon increasing wall thickness, the model predicted a switch-type behavior of the Notch signaling state with a steep transition of synthetic toward contractile VSMCs at a certain transition thickness. These thicknesses varied per investigated arterial location and were in good agreement with human anatomical data, thereby suggesting that the Notch response to hemodynamics plays an important role in the establishment of vascular homeostasis.

Indexed as

AgedArteriesBasic Helix-Loop-Helix ProteinsCell Cycle ProteinsComputer SimulationEndothelial CellsGene Expression RegulationHomeostasisHumansJagged-1 ProteinLigandsMechanotransduction, CellularMiddle AgedModels, BiologicalMorphogenesisMuscle ContractionBasic Helix-Loop-Helix ProteinsCell Cycle ProteinsHES1 protein, humanHEY1 protein, humanHEY2 protein, humanJAG1 protein, humanJagged-1 ProteinLigandsNOTCH3 protein, humanReceptor, Notch3Repressor ProteinsTranscription Factor HES-1homeostasisJaggedmechanosensitivityNotch

Identifiers

PMID29610298
PMCPMC5910818

What OpenQuestion holds

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Registered trials

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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.