Evidence map›Paper›PMID 31685999›Full record

ArticleNature biomedical engineering2020

Growth factors with enhanced syndecan binding generate tonic signalling and promote tissue healing.

Mayumi Mochizuki, Esra Güç, Anthony J Park, Ziad Julier, Priscilla S Briquez, Gisela A Kuhn, Ralph Müller, Melody A Swartz, Jeffrey A Hubbell, Mikaël M Martino

Abstract read
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In one paragraph

Article in Nature biomedical engineering, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 52 papers.

0numbers the graph read from it
0cells of the map it votes in
52citing 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

52 citing papers in PubMed.

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  8. Low-dose ionizing radiationMaterials today. Bio · 2025
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Mayumi MochizukiEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Clayton, Victoria, Australia.
Esra GüçInstitute of Bioengineering, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Anthony J ParkEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Clayton, Victoria, Australia.
Ziad JulierEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Clayton, Victoria, Australia.
Priscilla S BriquezInstitute of Bioengineering, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Gisela A KuhnInstitute for Biomechanics, ETH Zurich, Zürich, Switzerland.
Ralph MüllerInstitute for Biomechanics, ETH Zurich, Zürich, Switzerland.ORCID http://orcid.org/0000-0002-5811-7725
Melody A SwartzInstitute of Bioengineering, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Jeffrey A HubbellInstitute of Bioengineering, School of Life Sciences, Ecole Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.ORCID http://orcid.org/0000-0003-0276-5456
Mikaël M MartinoEuropean Molecular Biology Laboratory Australia, Australian Regenerative Medicine Institute, Monash University, Clayton, Victoria, Australia. mikael.martino@monash.edu.ORCID http://orcid.org/0000-0002-5012-4605

Funding

Engineering Growth Factor-ECM Interactions to Heal Chronic Wounds in Type 1 DiabetesDP3DK108215 · NIDDK · UNIVERSITY OF CHICAGO · PI HUBBELL, JEFFREY A. · 2015 to 2015
$1.5M
NIDDK NIH HHS DP3 DK108215
6 · The paper itself

Abstract

Growth factors can stimulate tissue regeneration, but the side effects and low effectiveness associated with suboptimal delivery systems have impeded their use in translational regenerative medicine. Physiologically, growth factor interactions with the extracellular matrix control their bioavailability and spatiotemporal cellular signalling. Growth factor signalling is also controlled at the cell surface level via binding to heparan sulfate proteoglycans, such as syndecans. Here we show that vascular endothelial growth factor-A (VEGF-A) and platelet-derived growth factor-BB (PDGF-BB) that were engineered to have a syndecan-binding sequence trigger sustained low-intensity signalling (tonic signalling) and reduce the desensitization of growth factor receptors. We also show in mouse models that tonic signalling leads to superior morphogenetic activity, with syndecan-binding growth factors inducing greater bone regeneration and wound repair than wild-type growth factors, as well as reduced tumour growth (associated with PDGF-BB delivery) and vascular permeability (triggered by VEGF-A). Tonic signalling via syndecan binding may also enhance the regenerative capacity of other growth factors.

Indexed as

AnimalsBecaplerminBone RegenerationCapillary PermeabilityCell MembraneCell ProliferationExtracellular MatrixHeparan Sulfate ProteoglycansHumansIntercellular Signaling Peptides and ProteinsMaleMiceMice, Inbred BALB CMice, Inbred C57BLMicrofluidicsModels, AnimalBecaplerminHeparan Sulfate ProteoglycansIntercellular Signaling Peptides and ProteinsNeuropilin-1Receptors, Growth FactorSyndecansVascular Endothelial Growth Factor A

Identifiers

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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.