4.7 Article

Identification of the long noncoding RNA NEAT1 as a novel inflammatory regulator acting through MAPK pathway in human lupus

期刊

JOURNAL OF AUTOIMMUNITY
卷 75, 期 -, 页码 96-104

出版社

ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/j.jaut.2016.07.012

关键词

Long noncoding RNA; NEAT1; TLR4; Systemic lupus erythematosus; Cytokines

资金

  1. National Basic Research Program of China (973 program) [2014CB541901, 2014CB541902]
  2. National Natural Science Foundation of China [81571576, 81230072, 31370880, 81421001]
  3. State Key Laboratory of Oncogenes and Related Genes [91-14-05]
  4. Key Research Program of the Chinese Academy of Sciences [KJZD-EW-L01-3]

向作者/读者索取更多资源

Long noncoding RNAs (IncRNAs) have recently been identified to be tightly linked to diverse human diseases. However, our knowledge of Systemic Lupus Erythematosus (SLE)-related lncRNAs remains limited. In the present study we investigated the contribution of the IncRNA NEAT1 to the pathogenesis of SLE. Here, we found NEAT1 expression was abnormally increased in SLE patients and predominantly expressed in human monocytes. Additionally, NEAT1 expression was induced by LPS via p38 activation. Silencing NEAT1 significantly reduced the expression of a group of chemokines and cytokines, including IL-6, CXCL10, etc., which were induced by LPS continuously and in late stages. Furthermore, it was identified the involvement of NEAT1 in TLR4-mediated inflammatory process was through affecting the activation of the late MAPK signaling pathway. Importantly, there was a positive correlation between NEAT1 and clinical disease activity in SLE patients. In conclusion, the increased NEAT1 expression may be a potential contributor to the elevated production of a number of cytokines and chemokines in SLE patients. Our findings suggest IncRNA contributes to the pathogenesis of lupus and provides potentially novel target for therapeutic intervention. (C) 2016 Elsevier Ltd. All rights reserved.

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。

评论

主要评分

4.7
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据