Evidence map›Paper›PMID 29289530›Full record

ArticleEBioMedicine2018

A Vascular Endothelial Growth Factor-Dependent Sprouting Angiogenesis Assay Based on an In Vitro Human Blood Vessel Model for the Study of Anti-Angiogenic Drugs.

Joris Pauty, Ryo Usuba, Irene Gayi Cheng, Louise Hespel, Haruko Takahashi, Keisuke Kato, Masayoshi Kobayashi, Hiroyuki Nakajima, Eujin Lee, Florian Yger and 2 more

Erratum issuedAbstract read
In one paragraph

Article in EBioMedicine, 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 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing 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

62 citing papers in PubMed.

  1. Trial
  2. 4D force patterning enables spatial control of angiogenesis.Proceedings of the National Academy of Sciences of the United States of America · 2026
    Article
  3. Review
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  10. Engineering in vitro vascular microsystems.Microsystems & nanoengineering · 2025
    Review
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  12. Article
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  15. Article
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  17. Article
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2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors.

Joris PautyCenter for International Research on Integrative Biomedical Systems (CIBiS), Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan; LIMMS/CNRS-IIS UMI 2820, Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan; CNRS/IIS/COL/Université Lille 1 SMMiL-E project, CNRS Délégation Nord-Pas de Calais et Picardie, 2 rue de Canonniers, Lille, Cedex 59046, France.
Ryo UsubaCenter for International Research on Integrative Biomedical Systems (CIBiS), Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan.
Irene Gayi ChengDepartment of Bioengineering, Clemson University, 118 Engineering Service Dr., Clemson, SC 29634, USA.
Louise HespelEcole Normale Supérieure-PSL Research University, Département de Chimie, Sorbonne Universités, UPMC Université Paris 06, CNRS UMR 8640 PASTEUR, 24 rue Lhomond, 75005 Paris, France.
Haruko TakahashiCenter for International Research on Integrative Biomedical Systems (CIBiS), Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan.
Keisuke KatoR&D Department 1, SCREEN Holdings Co., Ltd., 322 Furukawa-cho, Hazukashi, Fushimi-ku, Kyoto 612-8486, Japan.
Masayoshi KobayashiR&D Department 1, SCREEN Holdings Co., Ltd., 322 Furukawa-cho, Hazukashi, Fushimi-ku, Kyoto 612-8486, Japan.
Hiroyuki NakajimaDepartment of Cell Biology, National Cerebral and Cardiovascular Center Research Institute, Suita, Japan.
Eujin LeeCenter for International Research on Integrative Biomedical Systems (CIBiS), Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan.
Florian YgerLAMSADE, CNRS UMR 7243, Université Paris-Dauphine, PSL Research University, 75016 Paris, France.
Fabrice SoncinCNRS/IIS/COL/Université Lille 1 SMMiL-E project, CNRS Délégation Nord-Pas de Calais et Picardie, 2 rue de Canonniers, Lille, Cedex 59046, France; Université Lille, CNRS, Institut Pasteur de Lille, UMR 8161 - M3T, F-59000 Lille, France. Electronic address: fabrice.soncin@inserm.fr.
Yukiko T MatsunagaCenter for International Research on Integrative Biomedical Systems (CIBiS), Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan; LIMMS/CNRS-IIS UMI 2820, Institute of Industrial Science, The University of Tokyo, 4-6-1 Komaba, Meguro-ku, Tokyo 153-8505, Japan; CNRS/IIS/COL/Université Lille 1 SMMiL-E project, CNRS Délégation Nord-Pas de Calais et Picardie, 2 rue de Canonniers, Lille, Cedex 59046, France. Electronic address: mat@iis.u-tokyo.ac.jp.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Angiogenesis is the formation of new capillaries from pre-existing blood vessels and participates in proper vasculature development. In pathological conditions such as cancer, abnormal angiogenesis takes place. Angiogenesis is primarily carried out by endothelial cells, the innermost layer of blood vessels. The vascular endothelial growth factor-A (VEGF-A) and its receptor-2 (VEGFR-2) trigger most of the mechanisms activating and regulating angiogenesis, and have been the targets for the development of drugs. However, most experimental assays assessing angiogenesis rely on animal models. We report an in vitro model using a microvessel-on-a-chip. It mimics an effective endothelial sprouting angiogenesis event triggered from an initial microvessel using a single angiogenic factor, VEGF-A. The angiogenic sprouting in this model is depends on the Notch signaling, as observed in vivo. This model enables the study of anti-angiogenic drugs which target a specific factor/receptor pathway, as demonstrated by the use of the clinically approved sorafenib and sunitinib for targeting the VEGF-A/VEGFR-2 pathway. Furthermore, this model allows testing simultaneously angiogenesis and permeability. It demonstrates that sorafenib impairs the endothelial barrier function, while sunitinib does not. Such in vitro human model provides a significant complimentary approach to animal models for the development of effective therapies.

Indexed as

Biological AssayModels, BiologicalNeovascularization, PhysiologicAngiogenesis InhibitorsBlood VesselsGene Knockdown TechniquesHumansHuman Umbilical Vein Endothelial CellsIndolesMicrovesselsNiacinamidePhenylurea CompoundsPyrrolesSignal TransductionSorafenibSunitinibAngiogenesis InhibitorsIndolesNiacinamidePhenylurea CompoundsPyrrolesSorafenibSunitinibVascular Endothelial Growth Factor AAngiogenesis inhibitorsDLL4Human umbilical vein endothelial cellIn vitro 3D modelMicrovesselNotchSorafenibSprouting angiogenesisSunitinibVascular endothelial growth factor

Identifiers

PMID29289530
PMCPMC5828365

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.