期刊
ONCOTARGET
卷 7, 期 47, 页码 76667-76683出版社
IMPACT JOURNALS LLC
DOI: 10.18632/oncotarget.12395
关键词
miR-22; poly(I:C); type I interferon; inflammatory cytokines; MAVS
资金
- National Key Research and Development Program of China [2016YFD05004007]
- National Natural Sciences Foundation of China [31172325, 31472221]
- Special Fund for Agro-scientific Research in the Public Interest [201203082]
- Fundamental Research Funds for the Central University [2013PY051, 2662016Q003]
MicroRNAs (miRNAs) are small non-coding RNAs that play important roles in regulating the host immune response. Here we found that miR-22 is induced in glial cells upon stimulation with poly(I:C). Overexpression of miR-22 in the cultured cells resulted in decreased activity of interferon regulatory factor-3 and nuclear factor-kappa B, which in turn led to reduced expression of interferon-beta and inflammatory cytokines, including tumor necrosis factor-alpha, interleukin-1 beta, interleukin-6, and chemokine (C-C motif) ligand 5, upon stimulation with poly(I: C), whereas knockdown of miR-22 had the opposite effect. We used a combination of bioinformatics and experimental techniques to demonstrate that mitochondrial antiviral signaling protein (MAVS), which positively regulates type I interferon production, is a novel target of miR-22. Overexpression of miR-22 decreased the activity of a luciferase reporter containing the MAVS 3'-untranslated region and led to decreased MAVS mRNA and protein levels. In contrast, ectopic expression of miR-22 inhibitor led to elevated MAVS expression. Collectively, our results demonstrate that miR-22 negatively regulates poly(I:C)-induced production of type I interferon and inflammatory cytokines via targeting MAVS.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据