Lncrna NEAT1 Regulates Th1/Th2 in Pediatric Asthma by Targeting MicroRNA-217/GATA3

被引:1
|
作者
Yan, Xianpeng [1 ]
Liu, Hong [1 ]
Li, Ting [1 ]
机构
[1] Shaanxi Prov Peoples Hosp, Childrens Hosp, Xian 710068, Peoples R China
关键词
Pediatric asthma; Long noncoding RNAs; Immunology; Proteins; GLOBAL BURDEN; IFN-GAMMA; TH2; CELLS; GATA-3; EXPRESSION; CYTOKINES; BALANCE; RNA;
D O I
暂无
中图分类号
R1 [预防医学、卫生学];
学科分类号
1004 ; 120402 ;
摘要
Background: The imbalance of immune response between helper Th1 and Th2 cells is the direct cause of asthma. It was closely related to abnormal expression of lncRNAs. However, whether lncRNAs can regulate Th1/Th2 balance in pediatric asthma remains to be investigated. Methods: Peripheral blood samples were collected from children with asthma and normal volunteers at the Children's Hospital of Shaanxi Provincial People's Hospital (Xi'an, China) in 2020. The qRT-PCR was used to detect the expression of lncRNA NEAT1, miR-217 and GATA3 in peripheral blood samples. The effects of lncRNA NEAT1, miR-217, and GATA3 on CD4+T cell population were detected in vitro. Meanwhile, the regulatory effect of lncRNA NEAT1/miR-217/GATA3 was evaluated through the dual luciferase report assay, functional assays and animal experiments. Results: We investigated that lncRNA NEAT1 and GATA3 was significantly up-regulated in CD4+T cells in peripheral blood of children with asthma (P < 0.001). Knockdown of lncRNA NEAT1 or GATA3 significantly reduced Th2-related cytokines (P < 0.05), but had no effect on Th1 cells. Importantly, the interactions of lncRNA NEAT1 with miR-217 and miR-217 with GATA3 were confirmed by dual luciferase report assay. Meanwhile, functional assays and animal experiments demonstrated that lncRNA NEAT1 regulated GATA3 expression through sponge miR-217, thereby regulating Th1/Th2 balance in CD4+T cells in pediatric asthma. Conclusion: lncRNA NEAT1/miR-217/GATA3 axis may reveal the immunological mechanism of pediatric asthma, which has potential clinical application value in the future.
引用
收藏
页码:106 / 117
页数:12
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