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Abnormal miR-214/A20 expression might play a role in T cell activation in patients with aplastic anemia 被引量:1

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摘要 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 A2030 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.
出处 《Blood Science》 2020年第3期100-105,共6页 血液科学(英文)
基金 This study was supported by the National Natural Science Foundation of China(Nos 81370605,81702082,and 81460026) the Natural Science Foundation of Guangdong province(Nos S2012010008794,2017A030313852 and 2020A151501042) Science and Information Technology of Guangzhou funded basic research for application project(No 2014A020212209) Medical Scientific Research Foundation of Guangdong Province of China(No A20190346).
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