title: Mouse bone marrow-derived mesenchymal stem cells induce macrophage M2 polarization through the nuclear factor-κB and signal transducer and activator of transcription 3 pathways.
abstract: Increasing evidence has demonstrated that mesenchymal stem cells (MSCs)-mediated regulation of macrophages is critical for inflammation response and tissue injury repair. However, the underlying mechanism is not well understood. In this study, we investigated the effect of mouse bone marrow-derived MSCs on macrophages under normal and inflammatory conditions. Co-culture with MSCs or treatment with MSC-conditioned medium (MSC-CM) reduced the expression of tumor necrosis factor-α while inducing the expression of interleukin 10 (IL-10) and arginase 1 in lipopolysaccharide (LPS)-stimulated mouse RAW264.7 cells and splenic CD11b(+) cells. MSC-CM treatment increased the expression of CD206, a marker of alternatively activated M2 macrophages, in RAW264.7 cells. In addition, MSC-CM promoted the proliferation and migration of RAW264.7 cells. MSC-CM treatment activated signal transducer and activator of transcription 3 (STAT3) but inhibited nuclear factor-κB (NF-κB) pathways in LPS-stimulated RAW264.7 cells. Moreover, STAT3 inhibitor S3I-201 antagonized the induction of IL-10, arginase 1, and CD206 by MSC-CM in RAW264.7 cells. Conclusively, our findings suggest that mouse MSCs induce macrophage M2 activation through the NF-κB and STAT3 pathways.
authors: School of Medical Science and Laboratory Medicine, Jiangsu University, Zhenjiang, Jiangsu 212013, P. R. China.
authors: Shuo
authors: S
authors: Gao
authors: Fei
authors: F
authors: Mao
authors: Bin
authors: B
authors: Zhang
authors: Ling
authors: L
authors: Zhang
authors: Xu
authors: X
authors: Zhang
authors: Mei
authors: M
authors: Wang
authors: Yongmin
authors: Y
authors: Yan
authors: Tingting
authors: T
authors: Yang
authors: Jie
authors: J
authors: Zhang
authors: Wei
authors: W
authors: Zhu
authors: Hui
authors: H
authors: Qian
authors: Wenrong
authors: W
authors: Xu
mesh_terms: D000636:Aminosalicylic Acids / Q000494:pharmacology; D000818:Animals; D001119:Arginase / Q000096:biosynthesis / Q000378:metabolism; D001557:Benzenesulfonates / Q000494:pharmacology; D002465:Cell Movement; D049109:Cell Proliferation; D002478:Cells, Cultured; D016753:Interleukin-10 / Q000096:biosynthesis / Q000378:metabolism; D037181:Lectins, C-Type / Q000096:biosynthesis; D008070:Lipopolysaccharides; D008262:Macrophage Activation; D008264:Macrophages / Q000378:metabolism*; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins / Q000096:biosynthesis; D045164:Mesenchymal Stem Cell Transplantation; D059630:Mesenchymal Stem Cells / Q000378:metabolism*; D051379:Mice; D008807:Mice, Inbred BALB C; D011956:Receptors, Cell Surface / Q000096:biosynthesis; D050796:STAT3 Transcription Factor / Q000037:antagonists & inhibitors / Q000378:metabolism*; D015398:Signal Transduction; D051996:Transcription Factor RelA / Q000378:metabolism*; D014409:Tumor Necrosis Factor-alpha / Q000096:biosynthesis / Q000378:metabolism
chemical_list: D000636:Aminosalicylic Acids; D001557:Benzenesulfonates; C556062:IL10 protein, mouse; D037181:Lectins, C-Type; D008070:Lipopolysaccharides; D000090323:Mannose Receptor; D037241:Mannose-Binding Lectins; C520337:NSC 74859; D011956:Receptors, Cell Surface; C498144:Rela protein, mouse; D050796:STAT3 Transcription Factor; C494087:Stat3 protein, mouse; D051996:Transcription Factor RelA; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; C544448:Arg1 protein, mouse; D001119:Arginase
keywords: Mesenchymal stem cells; inflammation; macrophage; polarization; signaling pathway