CCL6 promotes M2 polarization and inhibits macrophage autophagy by activating PI3‐kinase/Akt signalling pathway during skin wound healing
Macrophage polarization
LY294002
M2 Macrophage
Phosphoinositide 3-kinase
DOI:
10.1111/exd.14718
Publication Date:
2022-12-02T07:57:29Z
AUTHORS (6)
ABSTRACT
The transition of macrophages from the proinflammatory M1 to anti-inflammatory M2 phenotype is crucial during wound healing process. In this study, we assess role chemokine (C-C motif) ligand 6 (CCL6) in modulating macrophage polarization and healing. Initially, observed significantly upregulated CCL6 expression skin tissue on edge inflammation proliferation phases. Furthermore, discovered that mice treated with rCCL6 had accelerated increased levels M2-type macrophages. Using vitro models, found promotes by activating PI3-kinase/Akt signalling pathway. Additionally, our results showed inhibited autophagy healing, whereas inducer rapamycin delayed Finally, determined PI3-kinase inhibitor LY294002 promoted decreased macrophages, indicating importance polarization, process was reversed CCL6. Taken together, study demonstrates inhibits autophagy, accelerates
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