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Oncotarget. 2017 Aug 24;8(44):77400-77406. doi: 10.18632/oncotarget.20490. eCollection 2017 Sep 29.

Long noncoding RNA MALAT-1 is a novel inflammatory regulator in human systemic lupus erythematosus.

Author information

1
Department of Rheumatology and Clinical Immunology, Clinical Immunology Center, The Ministry of Education Key Laboratory, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, China.
2
Department of Thoracic Surgery, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
3
Department of Pathology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Beijing, China.
4
National Key Laboratory of Molecular Oncology, Chinese Academy of Medical Sciences Cancer Hospital, Beijing, China.
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Contributed equally

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.

KEYWORDS:

IL-21; MALAT-1; PBMC; SLE; lncRNA

Conflict of interest statement

CONFLICTS OF INTEREST The authors declare no conflicts of interest.

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