Evidence map›Paper›PMID 37220183›Full record

ArticleScience signaling2023

Neuropilin-1 interacts with VE-cadherin and TGFBR2 to stabilize adherens junctions and prevent activation of endothelium under flow.

Emy Bosseboeuf, Anissa Chikh, Ahmed Bey Chaker, Tom P Mitchell, Dhilakshani Vignaraja, Ridhi Rajendrakumar, Rayomand S Khambata, Thomas D Nightingale, Justin C Mason, Anna M Randi and 2 more

Open access · greenAbstract read
In one paragraph

Article in Science signaling, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.

0numbers the graph read from it
0cells of the map it votes in
18citing papers in PubMed
4.3field-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

18 citing papers in PubMed, 28 citations in OpenAlex.

  1. Review
  2. Vascular mechanical forces and vascular diseases.Journal of advanced research · 2026
    Review
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  16. The role of TNC in atherosclerosis and drug development opportunities.International journal of biological sciences · 2024
    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

12 authors at 4 institutions in 2 countries.

Emy BosseboeufWilliam Harvey Research Institute, Barts and London School of Medicine and Dentistry, Centre of Cardiovascular Medicine and Devices, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.ORCID 0000-0001-5316-0508
Anissa ChikhMolecular and Clinical Sciences Research Institute, St. George's University of London, London SW17 0RE, UK.ORCID 0000-0002-4235-3870
Ahmed Bey ChakerWilliam Harvey Research Institute, Barts and London School of Medicine and Dentistry, Centre of Cardiovascular Medicine and Devices, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.ORCID 0000-0003-3373-2630
Tom P MitchellWilliam Harvey Research Institute, Barts and London School of Medicine and Dentistry, Centre for Microvascular Research, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.ORCID 0000-0003-2247-3098
Dhilakshani VignarajaNational Heart and Lung Institute, Imperial College London, London W12 0NN, UK.
Ridhi RajendrakumarWilliam Harvey Research Institute, Barts and London School of Medicine and Dentistry, Centre of Cardiovascular Medicine and Devices, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.ORCID 0000-0002-9606-7634
Rayomand S KhambataWilliam Harvey Research Institute, Barts and London School of Medicine and Dentistry, Centre of Cardiovascular Medicine and Devices, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Thomas D NightingaleWilliam Harvey Research Institute, Barts and London School of Medicine and Dentistry, Centre for Microvascular Research, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.
Justin C MasonVascular Sciences, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0HS, UK.
Anna M RandiVascular Sciences, National Heart and Lung Institute, Faculty of Medicine, Imperial College London, Hammersmith Campus, Du Cane Road, London W12 0HS, UK.ORCID 0000-0002-0729-211X
Amrita AhluwaliaWilliam Harvey Research Institute, Barts and London School of Medicine and Dentistry, Centre of Cardiovascular Medicine and Devices, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.ORCID 0000-0001-7626-6399
Claudio RaimondiWilliam Harvey Research Institute, Barts and London School of Medicine and Dentistry, Centre of Cardiovascular Medicine and Devices, Queen Mary University of London, Charterhouse Square, London EC1M 6BQ, UK.ORCID 0000-0002-1419-6855
William Harvey Research Institute · GBHammersmith Hospital · GBImperial College London · GBSt George's, University of London · GB

Funding

British Heart Foundation FS/16/22/32045
6 · The paper itself

Abstract

Linear and disturbed flow differentially regulate gene expression, with disturbed flow priming endothelial cells (ECs) for a proinflammatory, atheroprone expression profile and phenotype. Here, we investigated the role of the transmembrane protein neuropilin-1 (NRP1) in ECs exposed to flow using cultured ECs, mice with an endothelium-specific knockout of NRP1, and a mouse model of atherosclerosis. We demonstrated that NRP1 was a constituent of adherens junctions that interacted with VE-cadherin and promoted its association with p120 catenin, stabilizing adherens junctions and inducing cytoskeletal remodeling in alignment with the direction of flow. We also showed that NRP1 interacted with transforming growth factor-β (TGF-β) receptor II (TGFBR2) and reduced the plasma membrane localization of TGFBR2 and TGF-β signaling. NRP1 knockdown increased the abundance of proinflammatory cytokines and adhesion molecules, resulting in increased leukocyte rolling and atherosclerotic plaque size. These findings describe a role for NRP1 in promoting endothelial function and reveal a mechanism by which NRP1 reduction in ECs may contribute to vascular disease by modulating adherens junction signaling and promoting TGF-β signaling and inflammation.

Indexed as

Endothelial CellsNeuropilin-1Receptor, Transforming Growth Factor-beta Type IIAdherens JunctionsAnimalsCadherin 5CadherinsEndotheliumMiceCadherin 5CadherinsNeuropilin-1Receptor, Transforming Growth Factor-beta Type IITgfbr2 protein, mouse

Identifiers

PMID37220183
PMCPMC7614756
OpenAlexW4377711489

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.