Suppressed androgen receptor expression promotes M2 macrophage reprogramming through the STAT3/SOCS3 pathway

EXCLI Journal

Linlin Guo¹  Wenhan Ma²  Jingbo Zhang³ 

[1] Department of Internal Cardiology, the Second Hospital of Shandong University, Beiyuan Avenue 247#, Jinan, China. Tel: [phone], Fax:[phone], E-mail: [e-mail];Department of Internal Cardiology, the Second Hospital of Shandong University, Jinan, China;Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, China

关键词: myocarditis;    inflammation;    androgen receptor;    M2 macrophages;    SOCS3;    STAT3;   

DOI  :  10.17179/excli2018-1740

学科分类：过敏症与临床免疫学

来源: University of Mainz, University of Leipzig

【 摘 要 】

Macrophages are important mediators of inflammatory cardiovascular diseases, and various macrophage phenotypes exert opposite effects during inflammation. In our previous study, we proved that suppressed androgen receptor (AR) alleviated inflammation during experimental autoimmune myocarditis (EAM). As anti-inflammatory cells, whether M2 macrophages are involved in this process remains unclear. Here, we showed that anti-inflammatory cytokines and M2 macrophages were elevated when AR was suppressed during EAM. In IL-4 stimulation-induced M2 macrophages, impaired AR with ASC-J9 increased the expression of M2 macrophage-related factors. Moreover, suppressed AR expression resulted in macrophage M2 polarization by reducing SOCS3 production and enhancing STAT3 activation. Taken together, our data suggest that AR plays a critical role in macrophage polarization and suppressed redundant AR expression promotes anti-inflammatory M2 macrophages reprogramming. This study suggests a potential therapeutic agent for inflammatory cardiomyopathy through the use of ASC-J9.

【 授权许可】

CC BY