MicroRNA-326 Upregulates B Cell Activity and Autoantibody Production in Lupus Disease of MRL/lpr Mice

被引：25
|
作者：
Xia, Yuan [1 ]
Tao, Jin-Hui [1 ]
Fang, Xuan [1 ]
Xiang, Nan [1 ]
Dai, Xiao-Juan [1 ]
Jin, Li [1 ]
Li, Xiao-Mei [1 ]
Wang, Yi-Ping [2 ]
Li, Xiang-Pei [1 ]
机构：
[1] Anhui Med Univ, Anhui Prov Hosp, Dept Rheumatol & Immunol, 17 Lu Jiang Rd, Hefei 230001, Anhui, Peoples R China
[2] Univ Sydney, Westmead Inst Med Res, Ctr Transplantat & Renal Res, Sydney, NSW, Australia
来源：
MOLECULAR THERAPY-NUCLEIC ACIDS | 2018年 / 11卷
基金：
中国国家自然科学基金;
关键词：
AUTOIMMUNE-DISEASES; IMMUNE-RESPONSE; SLE PATIENTS; T-CELLS; ERYTHEMATOSUS; PATHOGENESIS; ETS-1; EXPRESSION; DIFFERENTIATION; NEPHRITIS;
D O I：
10.1016/j.omtn.2018.02.010
中图分类号：
R-3 [医学研究方法]; R3 [基础医学];
学科分类号：
1001 ;
摘要：
B cells are recognized as key participants in various autoimmune diseases, including systemic lupus erythematosus (SLE). Although sets of transcription factors and cytokines are known to regulate B cell differentiation, the roles of microRNAs are poorly understood. Our previous study proved that microRNA-326 (miR-326) was markedly upregulated in SLE patients; however, the biological function of miR-326 during SLE pathogenesis remained unknown. In this study, we found that miR-326 overexpression in MRL/lpr mice led to B cell hyperactivity and severe SLE. Moreover, E26 transformation-specific-1 (Ets-1), a negative regulator of B cell differentiation, was identified as a target of miR-326. Therefore, a novel mechanism has been found in which the elevated miR-326 in B cells of SLE promotes plasmablast development and antibody production through downregulation of Ets-1.
引用
收藏
页码：284 / 291
页数：8
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