MiR-183 delivery attenuates murine lupus nephritis-related injuries via targeting mTOR
MiR-183 delivery attenuates murine lupus nephritis-related injuries via targeting mTOR
复制标题
MiR-183 递送通过靶向 mTOR 减轻小鼠狼疮性肾炎相关损伤
DOI：
10.1111/sji.12810
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发表时间：
2019
影响因子：
3.7
通讯作者：
Luo Congjuan
中科院分区：
文献类型：
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作者：
Li Xiuzhen;Luo Feng;Li Jie;Luo Congjuan
microRNAs（miRNAs）在包括系统性红斑狼疮（SLE）在内的多种人类疾病的发生、发展中起着重要作用。SLE是一种自身免疫性疾病，其特征是产生针对核抗原的自身抗体和多器官受累。对参与SLE的miRNAs的研究为SLE的发病机制提供了新的见解，并可能导致新的治疗干预措施的确定。本研究的目的是通过使用MRL/lpr小鼠模型研究miR-183注射对SLE进展的影响。采用真实的实时定量PCR检测miR-183和mTOR mRNA的表达水平。通过向小鼠腹腔内注射miR-183，然后监测寿命、抗dsDNA抗体水平、尿白蛋白水平、血尿素氮（BUN）水平以及TcB和Th 17细胞群，检查miR-183对MRL/lpr小鼠自发性疾病进展过程的影响。我们发现，注射miR-183可降低抗DNA抗体和免疫复合物组分水平，恢复Tcl 4和Th 17细胞群并延长生存期。我们的研究结果表明，miR-183注射可作为延缓或缓解SLE病理特征的有效治疗方法。
MicroRNAs (miRNAs) play a vital role in the occurrence and development of many human diseases, including systemic lupus erythematosus (SLE). SLE is an autoimmune disease characterized by the production of autoantibodies against nuclear antigens and multiorgan involvement. Study of miRNAs involved in SLE provides new insights into the pathogenesis of SLE and might lead to the identification of new therapeutic interventions. The aim of this study was to investigate the effect of miR‐183 injection on the progression of SLE by using MRL/lpr mouse model. The expression levels of miR‐183 and mTOR mRNA were detected by quantitative real‐time PCR assay. The effect of miR‐183 on the course of spontaneous disease progression in the MRL/lpr mice was examined by intraperitoneal injection of miR‐183 into mice and followed by monitoring lifespan, anti‐dsDNA antibody levels, urinary albumin levels, blood urea nitrogen (BUN) levels, and Tregs and Th17 cell population. We found that miR‐183 injection resulted in reduction of anti‐DNA antibody and immune complex component levels, restoration of Tregs and Th17 cell population and prolongation of survival. Our findings suggest that miR‐183 injection may serve as an effective therapeutic treatment for delaying or easing pathologic features of SLE.