Fractalkine inhibits lipopolysaccharide-induced M1 polarization of macrophages by activating Wnt/β-catenin signaling pathway.
10.12122/j.issn.1673-4254.2020.12.05
- Author:
Qiming GONG
1
;
Yan JIANG
2
;
Junling LU
1
;
Yanwu YOU
1
Author Information
1. Department of Nephrology, Affiliated Hospital, Youjiang Medical University for Nationalities, Baise 533000, China.
2. Science Laboratory Center, Youjiang Medical University for Nationalities, Baise 533000, China.
- Publication Type:Journal Article
- Keywords:
Wnt/β-catenin signaling pathway;
fractalkine;
macrophages;
polarization
- MeSH:
Animals;
Chemokine CX3CL1;
Lipopolysaccharides/pharmacology*;
Macrophages;
Mice;
RAW 264.7 Cells;
Tumor Necrosis Factor-alpha;
Wnt Signaling Pathway
- From:
Journal of Southern Medical University
2020;40(12):1726-1731
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE:To explore the mechanism by which fractalkine (CX3CL1; FKN) inhibits lipopolysaccharide (LPS)-induced immunological response in RAW264.7 cells.
METHODS:A RAW264.7 cell model overexpressing FKN was established by transfection with the lentiviral vector CX3CL1. The effects of LPS, ICG-001 (a Wnt/β-catenin signaling pathway inhibitor), either alone or in combination, on M1 polarization of na?ve and FKN-overexpressing RAW264.7 cells were evaluated by detecting of intereukin-6 (IL-6) and tumor necrosis factor-α (TNF-
RESULTS:The RAW264.7 cell model of FKN overexpression was successfully established. In na?ve RAW264.7 cells, treatment with both ICG-001 and LPS, as compared with LPS alone, significant promoted TNF-
CONCLUSIONS:FKN overexpression suppresses LPS-induced M1 type polarization of RAW264.7 cells by activating Wnt/β-catenin signaling pathway.
