The function of DcR3.Fc and its derivatives in macrophage differentiation and skeletal muscle repair

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Presentation Time: 11:30 AM - 12:45 PM
Poster Board Number: B627
Abstract ID: 6152

Presenting Author:
Chao-Yuan Weng , student at Academia Sinica

Abstract:

Macrophages play a crucial role in regulating inflammation and tissue repair, influencing whether the tissue will regenerate or undergo fibrosis and dysfunction. However, the specific factors that can induce tissue repair/resolving macrophages remain unclear. Decoy receptor 3 (DcR3) is a soluble receptor without a transmembrane domain that can neutralize the effects of the tumor necrosis factor superfamily members FasL, LIGHT, and TL1A. In our previous study, we discovered that recombinant DcR3.Fc not only possesses neutralizing capabilities but also promotes M2-like macrophage differentiation. To delve deeper into its mechanisms, we created GRC2.Fc, which lacks the ligand-binding domain, thereby excluding the involvement of DcR3 ligands. Here, we observed that DcR3.Fc and GRC2.Fc induces differentiation of human CD14+ monocyte-derived macrophages and mouse bone marrow-derived macrophages toward a tissue repair/resolving phenotype in vitro. Furthermore, in a cardiotoxin-induced muscle injury model, intramuscular injection of GRC2.Fc protein promotes skeletal muscle repair and induce the expression of M2 macrophage markers in vivo. Our findings indicate that GRC2.Fc can induce macrophages toward a tissue repair/resolving phenotype and promote skeletal muscle repair.