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Galectin‐1 promotes an M2 macrophage response to polydioxanone scaffolds
Author(s) -
Abebayehu Daniel,
Spence Andrew,
Boyan Barbara D.,
Schwartz Zvi,
Ryan John J.,
McClure Michael J.
Publication year - 2017
Publication title -
journal of biomedical materials research part a
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.849
H-Index - 150
eISSN - 1552-4965
pISSN - 1549-3296
DOI - 10.1002/jbm.a.36113
Subject(s) - microbiology and biotechnology , materials science , regeneration (biology) , macrophage , polydioxanone , m2 macrophage , biology , biochemistry , in vitro , composite material
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.