Evidence map›Paper›PMID 42447931›Full record

ArticleJournal of controlled release : official journal of the Controlled Release Society2026

Phased affinity-controlled delivery of vascular endothelial growth factor, fibroblast growth factor-2, and platelet derived growth factor enhances in vitro angiogenesis.

Justin E Svendsen, Chandler L Asnes, Samuel R Nightheart, Madeleine R Ford, Armaan Hajarizadeh, Simon C Oh, Henry B Hochstatter, Johnathan R O'Hara-Smith, Robert E Guldberg, Marian H Hettiaratchi

Abstract read
In one paragraph

Article in Journal of controlled release : official journal of the Controlled Release Society, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. Review
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Justin E SvendsenKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States; Department of Chemistry and Biochemistry, University of Oregon, Eugene, OR 97403, United States; Institute of Molecular Biology, University of Oregon, Eugene, OR 97403, United States.
Chandler L AsnesKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States.
Samuel R NightheartKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States.
Madeleine R FordKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States; Department of Human Physiology, University of Oregon, Eugene, OR 97403, United States.
Armaan HajarizadehKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States; School of Computer and Data Sciences, University of Oregon, Eugene, OR 97403, United States.
Simon C OhKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States.
Henry B HochstatterKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States.
Johnathan R O'Hara-SmithInstitute of Molecular Biology, University of Oregon, Eugene, OR 97403, United States; Department of Biology, University of Oregon, Eugene, OR 97403, United States.
Robert E GuldbergKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States.
Marian H HettiaratchiKnight Campus for Accelerating Scientific Impact, University of Oregon, Eugene, OR 97403, United States; Department of Chemistry and Biochemistry, University of Oregon, Eugene, OR 97403, United States; Institute of Molecular Biology, University of Oregon, Eugene, OR 97403, United States. Electronic address: mhettiar@uoregon.edu.

Funding

MOLECULAR BIOLOGY AND BIOPHYSICST32GM007759 · NIGMS · UNIVERSITY OF OREGON · PI NOLEN, BRADLEY J · 1985 to 2021
$8.5M
Modulating Protein Activity in Tissue Repair using Engineered Affinity-based BiomaterialsR35GM147507 · NIGMS · UNIVERSITY OF OREGON · PI Marian Hirushika Hettiaratchi · 2022 to 2026
$2.0M
A Directed Evolution Approach to Affinity-Based Protein DeliveryR21EB032112 · NIBIB · UNIVERSITY OF OREGON · PI HETTIARATCHI, MARIAN HIRUSHIKA · 2021 to 2023
$602k
Development of affinity-based delivery systems for angiogenic growth factorsF31HL176164 · NHLBI · UNIVERSITY OF OREGON · PI Justin E Svendsen · 2024 to 2026
$147k
NHLBI NIH HHS F31 HL176164NIBIB NIH HHS R21 EB032112NIGMS NIH HHS R35 GM147507NIGMS NIH HHS T32 GM007759
6 · The paper itself

Abstract

Angiogenesis, the growth of vasculature from existing blood vessels, requires the coordinated secretion of multiple angiogenic growth factors that each stimulate the cellular recruitment, patterning, and morphogenesis inherent to vascular network formation. Among these secreted factors, vascular endothelial growth factor (VEGF), fibroblast growth factor-2 (FGF-2), and platelet derived growth factor (PDGF) amplify key stages of angiogenesis. Disruptions in their secretion have been implicated in poor vascular network formation. Current methods for exploring variations in the phased presentation of multiple different proteins are limited, which has restricted our ability to explore the effect of growth factor timing on angiogenesis. To address this knowledge gap, we developed affibodies, which are alpha-helical binding proteins, to phase the release of VEGF-165, FGF-2, and PDGF-BB from a single delivery vehicle via specific protein-affibody affinity interactions. We used yeast surface display to engineer three VEGF-, three FGF-2-, and two PDGF-specific affibodies with a wide range of affinities for their target proteins spanning dissociation constants of 3.08 ± 0.21 nM to 4550 ± 590 nM. We demonstrated that the cumulative release of VEGF and FGF-2 is inversely correlated with the strength of the protein-affibody affinity interaction and that hydrogels containing multiple protein-specific affibodies can control the release of VEGF, FGF-2, and PDGF, largely in accordance with the strength of the affinity interactions. Using a rat-derived intact microvascular fragment (MVF) model of in vitro angiogenesis, we revealed that sequential delivery of soluble VEGF, followed by FGF-2, and then PDGF enhances vascular network length by 2.8-fold and branching by 4.1-fold compared to untreated MVFs. We then designed an affibody-conjugated polyethylene glycol maleimide (PEG-MAL) hydrogel to mimic this sequence of protein delivery, resulting in a 3.0-fold increase in vascular network length and a 2.3-fold increase in vascular branching compared to all other hydrogel compositions and the sequential delivery of soluble growth factors. Changing temporal growth factor presentation with affibody-conjugated hydrogels altered the expression of key angiogenic genes involved in vessel stabilization and destabilization and matrix remodeling. Perivascular coverage measured by the colocalization of lectin and alpha smooth muscle actin staining was similar between all treatment groups, suggesting pericyte recruitment to stabilize expanded vascular networks created by the soluble and affibody-mediated delivery of the optimal sequence of proteins. Overall, this work establishes a new biomaterial platform for modulating the timing of growth factor delivery, enabling the exploration of how temporal variations in protein secretion impact regeneration and development.

Indexed as

AngiogenesisFibroblast Growth Factor 2Neovascularization, PhysiologicPlatelet-Derived Growth FactorVascular Endothelial Growth Factor AAnimalsBecaplerminDelayed-Action PreparationsHumansHuman Umbilical Vein Endothelial CellsRecombinant Fusion ProteinsBecaplerminDelayed-Action PreparationsFibroblast Growth Factor 2Platelet-Derived Growth FactorRecombinant Fusion ProteinsVascular Endothelial Growth Factor AAffinity interactionsAngiogenesisDrug deliveryFGF-2PDGFVascular morphologyVEGF

Identifiers

PMID42447931
PMCPMC13451053

What Socratic 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 Socratic graph.