Metformin inhibits the immune functions of immature dendritic cells by regulating F-actin remodeling
10.19405/j.cnki.issn1000–1492.2026.03.013
- VernacularTitle:二甲双胍通过影响F-actin重构抑制未成熟树突状细胞的免疫功能
- Author:
Xianmei LIU
1
;
Zhimei CHENG
1
;
Enjie ZHOU
1
;
Juanyong LI
1
;
Yijun JIN
1
;
Liming ZHOU
1
;
Min XU
1
Author Information
1. Department of Interventional Radiology， Affiliated Hospital of Guizhou Medical University， Guiyang 550004
- Publication Type:Journal Article
- Keywords:
immature dendritic cells;
metformin;
antigen capturing ability;
F-actin remodeling;
CD205;
RhoA-ROCK-LIMK-Cofilin signaling pathway
- From:
Acta Universitatis Medicinalis Anhui
2026;61(3):480-486
- CountryChina
- Language:Chinese
-
Abstract:
ObjectiveTo investigate the effects of metformin on the immune functions of immature dendritic cells （imDCs） and the underlying mechanisms. MethodsMouse bone marrow-derived imDCs were treated with different concentrations of metformin. The working concentration and treatment time of metformin in this study were determined based on the results of cell apoptosis and cell viability assays. The effects of metformin on the phagocytic capacity of imDCs was evaluated using an antigen endocytosis assay. The expression of cluster of differentiation 205 （CD205）， the polymerization of filamentous actin （F-actin）， and the underlying regulatory mechanisms were investigated through flow cytometry， laser confocal fluorescence microscopy， and Western blot. ResultsThe working concentrations of metformin were 1， 2， 4 mmol/L for 24 h determined by the apoptosis and cell viability assays.Metformin significantly suppressed the phagocytic capacity of imDCs， down-regulated the expression of the mannose receptor CD205 on the cell surface， which was closely associated with phagocytic function； metformin inhibited the RhoA-ROCK1-LIMK1-Cofilin signaling pathway， which inhibited the polymerization of F-actin and disturbed its dynamic remodeling of imDCs. ConclusionMetformin can inhibit the expression of CD205 and disrupt the remodeling of F-actin， thereby suppressing the antigen-capturing capacity of imDCs.
