Evidence map›Paper›PMID 28544348›Full record

ArticleJournal of biomedical materials research. Part A2017

Galectin-1 promotes an M2 macrophage response to polydioxanone scaffolds.

Daniel Abebayehu, Andrew Spence, Barbara D Boyan, Zvi Schwartz, John J Ryan, Michael J McClure

Open access · greenAbstract read
In one paragraph

Article in Journal of biomedical materials research. Part A, 2017. 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
1.2field-weighted citation impact, top 22% 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, 35 citations in OpenAlex.

  1. Healing mechanisms of Galectin-1 in the ischemic heart.Cell biochemistry and biophysics · 2026
    Review
  2. Review
  3. Biological responses to biomaterials: a review.Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica · 2025
    Review
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  8. Review
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  13. Lipidome profiling with Raman microspectroscopy identifies macrophage response to surface topographies of implant materials.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Article
  15. Progress on Modulating Tumor-Associated Macrophages with Biomaterials.Advanced materials (Deerfield Beach, Fla.) · 2020
    Review
  16. Article
  17. Article
  18. Article
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

6 authors at 2 institutions in 1 country.

Daniel AbebayehuDepartment of Biology, Virginia Commonwealth University, Richmond, Virginia.
Andrew SpenceDepartment of Biology, Virginia Commonwealth University, Richmond, Virginia.
Barbara D BoyanDepartment of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, Virginia.
Zvi SchwartzDepartment of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, Virginia.
John J RyanDepartment of Biology, Virginia Commonwealth University, Richmond, Virginia.
Michael J McClureDepartment of Biomedical Engineering, School of Engineering, Virginia Commonwealth University, Richmond, Virginia.
Virginia Commonwealth University · USThe University of Texas at San Antonio · US

Funding

IL-10 Regulates Mast Cell Function and SurvivalR01AI059638 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI RYAN, JOHN J · 2007 to 2017
$3.8M
Control of IgG-mediated Inflammation by Fyn and Lyn KinasesR01AI101153 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI RYAN, JOHN J · 2013 to 2017
$2.0M
Regulation of Mast Cell Homeostasis by Interleukin-10R56AI059638 · NIAID · VIRGINIA COMMONWEALTH UNIVERSITY · PI RYAN, JOHN J · 2005 to 2005
$332k
NIAID NIH HHS R01 AI059638NIAID NIH HHS R01 AI101153NIAID NIH HHS R56 AI059638
6 · The paper itself

Abstract

Regulating soft tissue repair to prevent fibrosis and promote regeneration is central to creating a microenvironment conducive to soft tissue development. Macrophages play an important role in this process. The macrophage response can be modulated using biomaterials, altering cytokine and growth factor secretion to promote regeneration. Electrospun polydioxanone (PDO) fiber scaffolds promoted an M2 phenotype when macrophages were cultured on large diameter, highly porous scaffolds, but an M1 phenotype on smaller diameter fibers. In this study, we investigated whether incorporation of galectin-1, an immunosuppressive protein that enhances muscle regeneration, could promote the M2 response. Galectin-1 was incorporated into large and small fiber PDO scaffolds during electrospinning. Galectin-1 incorporation increased arginase-1 and reduced iNOS and IL-6 production in mouse bone-marrow derived macrophages compared with PDO alone for both scaffold types. Inhibition of ERK mitogen-activated protein kinase did not alter galectin-1 effects on arginase-1 and iNOS expression, but reversed IL-6 suppression, indicating that IL-6 is mediated by a different mechanism. Our results suggest that galectin-1 can be used to modulate macrophage commitment to a pro-regenerative M2 phenotype, which may positively impact tissue regeneration when using small diameter PDO scaffolds. © 2017 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 105A: 2562-2571, 2017.

Indexed as

AnimalsArginaseCytokinesExtracellular Signal-Regulated MAP KinasesFemaleGalectin 1Inflammation MediatorsMacrophagesMaleMice, Inbred C57BLNitric Oxide Synthase Type IIPhenotypePolydioxanoneSolubilityTissue ScaffoldsArginaseCytokinesExtracellular Signal-Regulated MAP KinasesGalectin 1Inflammation MediatorsNitric Oxide Synthase Type IIPolydioxanonegalectin-1immunomodulationmacrophagepolydioxanone

Identifiers

PMID28544348
PMCPMC5563977
OpenAlexW2626274186

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.