Investigation of MicroRNA in Mitochondrial Apoptotic Pathway in Systemic Lupus Erythematosus

系统性红斑狼疮中线粒体凋亡通路中microRNA的研究

阅读:1

Abstract

BACKGROUND: Accumulating evidence indicates that microRNAs play a pivotal role in the pathogenesis of systemic lupus erythematosus (SLE). This study tested the hypothesis that microRNA is associated with the mitochondrial apoptotic pathway in patients with SLE. METHODS: Thirteen patients were in the clinical comparison study and microRNA study and overall 19 patients in the study of intracellular protein. Levels of microRNAs were determined by miRNeasy kit in 13 patients with SLE and 29 volunteer normal controls. Intracellular levels of caspase-9, caspase-10, MAVS, MDA5, and pIRF7 in mononuclear cells from 19 patiens and the SLE disease activity index (SLEDAI) were determined in all SLE patients. Correlation analyses were performed among microRNAs, intracellular adaptor proteins, and caspase levels and mean SLEDAI. RESULTS: The ΔCT, defined by test reading difference between the target and the internal control microRNA (miR-451a), of miR-21-5p, miR-150-5p, and miR221-3p were significantly higher in plasma from SLE patients than in normal controls. miR-150-5pΔCT was positively correlated with both CRP and SLEDAI value. miR-150-5pΔCT was negatively associated with MAVS 70 kD. Caspase-10 protein levels were negatively associated with plasma miR-22-3pΔCT and miR-21-5pΔCT levels. CONCLUSIONS: Our study confirmed the hypothesis that these microRNAs were associated with the mitochondrial apoptotic pathway in SLE. miR-150-5pΔCT was positively associated with SLE disease activity and it was negatively correlated with MAVS 70 kD, which may facilitate viral survival and further enhance inflammation. On the other hand, miR-22-3pΔCT and miR-21-5pΔCT, were negatively correlated with caspase-10 levels, which may repress extrinsic apoptosis and increase cell survival.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。