Journal
EXPERIMENTAL CELL RESEARCH
Volume 357, Issue 2, Pages 155-162Publisher
ELSEVIER INC
DOI: 10.1016/j.yexcr.2017.05.010
Keywords
JNK; Alternatively activation; IL-4; Macrophage
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Funding
- National Natural Science Foundation of China [31401191]
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It has been generally accepted that alternatively activated macrophages (M2), which can be induced by type 2 cytokines such as IL-4, is responsible for tissue repair. However, the function of INK in IL-4-induced M2 macrophage polarization remains unclear. Here, we demonstrated that MO macrophages can be polarized into M2 status in response to IL-4 stimulation with the increased expression of the M2-specific molecular markers. We also found that IL-4 induced higher expression of JNK and transcription factor c-Myc in M2 macrophages. Our Q-PCR and Western blot results showed that JNK increased the expression of c-Myc and M2 markers Argl, Mrcl. We also demonstrated c-Myc was the downstream of IL-4-JNK pathway. Further, the depletion of c-Myc, Argl and Mrcl could inhibit the migration ability of M2 macrophages. Taken together, our data establishes a new role for JNK signaling in IL-4-induced alternative activation of macrophages and may provide a novel strategy for immune therapy.
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