Altered microRNA expression profile with miR-146a upregulation in CD4+T cells from patients with rheumatoid arthritis

Jingyi Li(Army Medical University), Ying Wan(Army Medical University), Qiuye Guo(Army Medical University), Liyun Zou(Army Medical University), Jinyu Zhang(Army Medical University), Yongfei Fang(Army Medical University), Jingbo Zhang(Army Medical University), Jinjun Zhang(Army Medical University), Xiaolan Fu(Army Medical University), Hongli Liu(Army Medical University), Liwei Lu(University of Hong Kong), Yuzhang Wu(Army Medical University)
Arthritis Research & Therapy
May 11, 2010
Cited by 252Open Access
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Abstract

INTRODUCTION: Increasing evidence indicates that microRNAs (miRNAs) play a critical role in the pathogenesis of inflammatory diseases. The aim of the study was to investigate the expression pattern and function of miRNAs in CD4+ T cells from patients with rheumatoid arthritis (RA). METHODS: The expression profile of miRNAs in CD4+ T cells from synovial fluid (SF) and peripheral blood of 33 RA patients was determined by microarray assay and validated by qRT-PCR analysis. The correlation between altered expression of miRNAs and cytokine levels was determined by linear regression analysis. The role of miR-146a overexpression in regulating T cell apoptosis was evaluated by flow cytometry. A genome-wide gene expression analysis was further performed to identify miR-146a-regulated genes in T cells. RESULTS: miRNA expression profile analysis revealed that miR-146a expression was significantly upregulated while miR-363 and miR-498 were downregulated in CD4+ T cells of RA patients. The level of miR-146a expression was positively correlated with levels of tumor necrosis factor-alpha (TNF-alpha), and in vitro studies showed TNF-alpha upregulated miR-146a expression in T cells. Moreover, miR-146a overexpression was found to suppress Jurkat T cell apoptosis. Finally, transcriptome analysis of miR-146a overexpression in T cells identified Fas associated factor 1 (FAF1) as a miR-146a-regulated gene, which was critically involved in modulating T cell apoptosis. CONCLUSIONS: We have detected increased miR-146a in CD4+ T cells of RA patients and its close correlation with TNF-alpha levels. Our findings that miR-146a overexpression suppresses T cell apoptosis indicate a role of miR-146a in RA pathogenesis and provide potential novel therapeutic targets.


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