TRIM24 alleviates viral myocarditis by promoting STAT6 phosphorylation-mediated macrophage M2 polarization
10.3969/j.issn.1000-484X.2024.08.005
- VernacularTitle:TRIM24调控STAT6磷酸化介导的巨噬细胞M2极化缓解病毒性心肌炎
- Author:
Liangyu ZHU
1
;
Xueqin LI
;
Xin ZHANG
;
Guoquan YIN
;
Yuan ZHANG
;
Kun LYU
Author Information
1. 皖南医学院第一附属医院弋矶山医院中心实验室,芜湖 241001
- Keywords:
TRIM24;
Macrophage polarization;
Viral myocarditis
- From:
Chinese Journal of Immunology
2024;40(8):1595-1600,1606
- CountryChina
- Language:Chinese
-
Abstract:
Objective:To study the role and preliminary molecular mechanism of TRIM24 regulating macrophage polarization in viral myocarditis(VM).Methods:VM mouse model was established by Coxsackie virus B3(CVB3),and expression of TRIM24 in myocardial tissue was detected.Cardiac inflammation level and polarization phenotype of cardiac infiltrating macrophages in a murine model of cardiac TRIM24 inhibition were detected in vivo.A polarization model of mouse bone marrow-derived macrophages(BMDMs)in vitro was established to observe the role of TRIM24 inhibition in polarizing BMDMs to M1 and M2,as well as its effects on phagocy-tosis and bactericidal function of BMDMs.Effects of TRIM24 inhibition on total STAT6 protein level and phosphorylation were investi-gated.Results:TRIM24 was significantly highly expressed in myocardial tissue of VM mice(P<0.001).Inhibition of TRIM24 expres-sion in myocardium had an attenuating effect on VM and promoted polarization of cardiac infiltrating macrophages to M2.TRIM24 was significantly down-regulated in vitro during the polarization of BMDMs toward M2(P<0.01).Inhibition of TRIM24 expression signifi-cantly promoted macrophage polarization toward M2 type and inhibited polarization toward M1 type,accompanied by a significant increase in STAT6 phosphorylation levels(P<0.01).Conclusion:TRIM24 regulates macrophage M2 polarization via activation of STAT6 signaling pathway to attenuate VM.
