Abstract |
Despite growing evidence that Long noncoding RNAs (lncRNAs) can regulate gene expression and widely take part in autoimmune and inflammatory diseases, our knowledge of systemic lupus erythematosus (SLE)-related lincRNAs remains limited. In this study, we aimed to explore the contribution of the lncRNA metastasis associated lung adenocarcinoma transcript 1 (MALAT1) to the pathogenesis of SLE. PBMCs were obtained from SLE patients and healthy donors. The expression levels of MALAT-1 were measured by quantitative PCR. Small interfering RNA ( siRNA) was then used to knock down the expression of MALAT1 in order to determine the role of MALAT1 in the expression levels of IL-21 and SIRT1 signaling pathway in primary monocytes of SLE patients. Here, we found MALAT-1 expression was abnormally increased in SLE patients and predominantly expressed in human monocytes. Additionally, silencing MALAT-1 significantly reduced the expression of IL-21 in primary monocytes of SLE patients. Furthermore, MALAT-1 exerts its detrimental effects by regulating SIRT1 signaling. Our results demonstrate that MALAT-1 is the key regulatory factor in the pathogenesis of SLE and provides potentially novel target for therapeutic intervention.
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Authors | Huaxia Yang, Naixin Liang, Min Wang, Yunyun Fei, Jian Sun, Zhiyuan Li, Yuan Xu, Chao Guo, Zhili Cao, Shanqing Li, Yuchen Jiao |
Journal | Oncotarget
(Oncotarget)
Vol. 8
Issue 44
Pg. 77400-77406
(Sep 29 2017)
ISSN: 1949-2553 [Electronic] United States |
PMID | 29100395
(Publication Type: Journal Article)
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