中国免疫学杂志2024，Vol.40Issue(8)：1595-1600,1606,7.DOI:10.3969/j.issn.1000-484X.2024.08.005
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
TRIM24 alleviates viral myocarditis by promoting STAT6 phosphorylation-mediated macrophage M2 polarization
摘要
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.关键词
TRIM24/巨噬细胞极化/病毒性心肌炎Key words
TRIM24/Macrophage polarization/Viral myocarditis分类
医药卫生引用本文复制引用
朱良宇,李雪琴,张欣,殷国泉,张苑,吕坤..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[J].中国免疫学杂志,2024,40(8):1595-1600,1606,7.基金项目
国家自然科学基金(82072370) （82072370）
安徽省自然科学基金杰青项目(2108085J44). （2108085J44）
