FOXP3型
外周血单个核细胞
基因敲除
白细胞介素2受体
流式细胞术
生物
调节性T细胞
免疫学
肾病
内分泌学
内科学
医学
免疫系统
T细胞
细胞培养
体外
糖尿病
生物化学
遗传学
作者
Lingwei Jin,Han-Yang Ye,Xiaoyan Xu,Yu Zheng,Yan Chen
标识
DOI:10.1016/j.biopha.2018.02.022
摘要
The aim of this study was to investigate the effect of miR-133a and miR-133b on regulatory T cell (Treg) differentiation in IgA nephropathy (IgAN) through targeting forkhead box P3 (FOXP3).Peripheral blood mononuclear cells (PBMCs) were isolated from IgAN patients (n = 20) and healthy controls (n = 20). Percentage of Tregs defined as CD4 + CD25 + FOXP3 + T cells were determined by flow cytometry. The mRNA expression levels of miR-133a, miR-133b and FOXP3 were measured by real-time PCR. FOXP3 protein level was analyzed by western blotting.Tregs percentage in PBMCs of IgAN patients was significantly lower than that of healthy controls, whereas the expression levels of miR-133a and miR-133b in IgAN patients were dramatically higher than that in the control group. Treg percentage was negatively correlated with miR-133a and miR-133b expressions. Meanwhile, miR-133a and miR-133b modulated FOXP3 expression by detecting of its gene 3'-untranslated region. MiR-133a or miR-133b overexpression significantly decreased the % Tregs (CD4 + CD25 + FOXP3+) of the total CD4 + T cells while miR-133a or miR-133b knockdown led to an opposite effect. Moreover, FOXP3 levels in IgAN patients was significantly lower than that in the control group and was negatively correlated with miR-133a and miR-133b expression.MiR-133a and miR-133b inhibited Treg differentiation in IgA nephropathy through targeting FOXP3.
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