SOCS3 Is Upregulated and Targeted by miR30a-5p in Allergic Rhinitis

被引:17
|
作者
Zhao, Chun Yuan [1 ]
Wang, Wei [1 ]
Yao, Hong Chao [1 ]
Wang, Xin [1 ]
机构
[1] Harbin Med Univ, Hosp 2, Dept Otorhinolaryngol & Head & Neck Surg, Xuefu Rd 246, Harbin 150086, Heilongjiang, Peoples R China
关键词
Allergic rhinitis; SOCS3; SOCS1; miR30a; CYTOKINE SIGNALING 1; T-CELLS; INFLAMMATORY ARTHRITIS; CHRONIC RHINOSINUSITIS; AIRWAY INFLAMMATION; ATOPIC-DERMATITIS; NASAL-MUCOSA; IFN-GAMMA; IN-VIVO; EXPRESSION;
D O I
10.1159/000486857
中图分类号
R392 [医学免疫学];
学科分类号
100102 ;
摘要
Background: Suppressor of cytokine signaling 1 (SOCS1) and SOCS3 play important roles in T helper cell differentiation, which is involved with the pathologic mechanisms of allergic rhinitis (AR). The aim of this study was to evaluate the expression of SOCS1 and SOCS3 in AR and find their regulatory microRNAs (miRNAs) to provide a basis for the treatment of AR. Methods: The expression of SOCS1 and SOCS3 were analyzed by real-time PCR, immunohistochemistry, and Western blot. The correlative regulatory miRNAs were detected by real-time PCR. Luciferase assays and AR mouse model experiments were applied to identify correlative miRNAs that target SOCS3. Results: SOCS1 and SOCS3 mRNA were upregulated in the nasal mucosa and peripheral blood mononuclear cells of AR compared with controls. The expression of SOCS3 protein was significantly increased in the nasal mucosa of AR. The immunohistochemical staining results showed that SOCS3 was similarly localized in the superficial epithelium, submucosal glands, and vascular endothelium in the nasal mucosa of AR subjects and controls. However, SOCS3 protein was especially localized in the inflammatory cells, such as eosinophils, monocytes, and lymphocytes. Conclusions: SOCS3 was targeted by miR30a-5p in AR. Further study should be performed to identify the regulatory effect of miR30a-5p in AR, which may provide insights into a new therapeutic strategy. (C) 2018 S. Karger AG, Basel
引用
收藏
页码:209 / 219
页数:11
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