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Remote Manipulation of Slidable Nano‐Ligand Switch Regulates the Adhesion and Regenerative Polarization of Macrophages
Author(s) -
Choi Hyojun,
Bae Gunhyu,
Khatua Chandra,
Min Sunhong,
Jung Hee Joon,
Li Na,
Jun Indong,
Liu HuiWen,
Cho Youngkyu,
Na KyuHwan,
Ko Minji,
Shin Hongchul,
Kim Yoon Hyuck,
Chung Seok,
Song JaeJun,
Dravid Vinayak P.,
Kang Heemin
Publication year - 2020
Publication title -
advanced functional materials
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.069
H-Index - 322
eISSN - 1616-3028
pISSN - 1616-301X
DOI - 10.1002/adfm.202001446
Subject(s) - materials science , ligand (biochemistry) , adhesion , biophysics , nanotechnology , extracellular matrix , microbiology and biotechnology , chemistry , biology , receptor , biochemistry , composite material
The development of materials capable of varying macroscale ligand distributions can emulate an extracellular matrix (ECM) remodeling and regulate the adhesion and polarization of macrophages. In this report, negatively charged slidable nano‐ligands are assembled and then conjugated to a positively charged substrate via electrostatic interaction. The negatively charged slidable nano‐ligands are prepared by coating magnetic nanoparticles with a polymer linker and negatively charged RGD ligand. The nano‐ligand sliding is characterized under an external magnetic field, which spatiotemporally alters macroscale ligand density. To the best of knowledge, this is the first demonstration that magnetic maipulation of the macroscale ligand density inhibits inflammatory M1 phenotype but stimulates the adhesion and regenerative M2 phenotype of host macrophages. Furthermore, it is elucidated that the magnetic attraction of the slidable nano‐ligand facilitates the assembly of adhesion structures in macrophages, thereby stimulating their regenerative M2 phenotype. The design of ECM‐emulating materials that allow remote, spatiotemporal, and reversible controllability of macroscale ligand density provides an appealing strategy in the spatiotemporal regulation of immunomodulatory tissue‐regenerative responses to implants in vivo.