Open AccessAbnormal miR-214/A20 expression might play a role in T cell activation in patients with aplastic anemia
Author(s) -
Zhi Yu,
Cunte Chen,
Yankai Xiao,
Xiaohui Chen,
Lixing Guo,
Guangxiao Tan,
Guixuan Huang,
Weifeng Luo,
Ming Zhou,
Yumiao Li,
Lin Chen,
Qi Shen,
Yuping Zhang,
Bo Li
Publication year - 2020
Publication title -
blood science
Language(s) - English
Resource type - Journals
ISSN - 2543-6368
DOI - 10.1097/bs9.0000000000000053
Subject(s) - aplastic anemia , microrna , peripheral blood mononuclear cell , pathogenesis , t cell , immunology , gene expression , real time polymerase chain reaction , luciferase , gene , biology , cancer research , medicine , microbiology and biotechnology , bone marrow , transfection , genetics , immune system , in vitro
Aberrant T cell activation is a major cause of aplastic anemia (AA) pathogenesis. Recent studies have shown that miRNAs regulate T cell activation and are involved in AA. A previous study found that miR-214 was significantly up-regulated upon T cell activation in a CD28-dependent fashion by targeting PTEN. However, the expression characteristics of miR-214 and its target genes in AA have not been defined. In this study, target genes for miR-214 were predicted and confirmed by bioinformatics and luciferase reporter assays. The expression levels of miR-214 and target genes were detected in 36 healthy individuals and 35 patients with AA in peripheral blood mononuclear cells by real-time quantitative reverse transcriptase-polymerase chain reaction. Bioinformatics and luciferase reporter assays identified that miR-214 could bind to the A20 3' untranslated regions. Significantly increased miR-214 and the decreased A20 expression level were detected in the AA patients compared with the healthy group. In addition, significantly increased miR-214 was found in non-severe aplastic anemia compared with severe aplastic anemia patients. These results suggested that the A20 gene was a potential target of miR-214, and elevated miR-214 might medicate T cell activation at least in part by regulating A20 expression in AA. We firstly confirmed that miR-214 regulated A20 expression, and aberrant miR-214/A20 expression might contribute to immunopathology in AA. The miR-214 expression might be used as a potential biomarker that assisted in diagnosing AA severity.