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The role of microRNA-16 in the pathogenesis of autoimmune diseases: A comprehensive review

Authors :
Lan Yan
Mingge Liang
Xiaoqiang Hou
Yiwen Zhang
Haoran Zhang
Zhe Guo
Ji Jinyu
Zhitao Feng
Zhigang Mei
Source :
Biomedicine & Pharmacotherapy, Vol 112, Iss , Pp - (2019)
Publication Year :
2019
Publisher :
Elsevier, 2019.

Abstract

MicroRNAs (miRNAs) are a class of small noncoding RNAs that are only 21–25 nt long. Many studies have shown that miRNA dysfunction is closely related to the occurrence and development of diseases. By combining with the 3′ noncoding region of target gene mRNA, miRNAs can mediate the degradation or translation inhibition of mRNA and exert a powerful regulation effect on gene expression at the posttranscriptional level, mainly inhibiting the translation or degradation of targets. Therefore, they are a class of molecules that play a negative regulatory role. Current studies have found that miR-16 is closely related to the occurrence of several autoimmune diseases. Studies have reported that miR-16 participates in the occurrence and development of rheumatoid arthritis, systemic lupus erythematosus, ankylosing spondylitis, inflammatory bowel disease, autoimmune thyroid disease, juvenile idiopathic arthritis, primary Sjogren's syndrome and other autoimmune diseases by regulating the expression of cytokines such as TNF-α, IL-8, IL-6, and IL-4; regulating activin A receptor (ACVR), growth differentiation factor-5 (GDF-5) and adenosine A2a receptor (A2AR) expression; affecting the proliferation, differentiation of Th17 cells and Treg cells; and regulating the balance between the cells. In this review, emphasis will be placed on the recent progress in characterizing the roles of miR-16 in these autoimmune diseases.

Details

Language :
English
ISSN :
07533322
Volume :
112
Issue :
-
Database :
Directory of Open Access Journals
Journal :
Biomedicine & Pharmacotherapy
Publication Type :
Academic Journal
Accession number :
edsdoj.3d7704e5676548ec91dfa8d78502fd82
Document Type :
article
Full Text :
https://doi.org/10.1016/j.biopha.2019.01.044