Document Detail


Decreased microRNA(miR)-145 and increased miR-224 expression in T cells from patients with systemic lupus erythematosus involved in lupus immunopathogenesis.
MedLine Citation:
PMID:  23199328     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with abnormal T cell immune responses. We hypothesized that aberrant expression of microRNAs (miRNAs) in T cells may contribute to the pathogenesis of SLE. First, we analysed the expression profiles of 270 human miRNAs in T cells from five SLE patients and five healthy controls and then validated those potentially aberrant-expressed miRNAs using real-time polymerase chain reaction (PCR). Then, the expression of mRNAs regulated by these aberrant-expressed miRNAs was detected using real-time PCR. Finally, miRNA transfection into Jurkat T cells was conducted for confirming further the biological functions of these miRNAs. The initial analysis indicated that seven miRNAs, including miR-145, miR-224, miR-513-5p, miR-150, miR-516a-5p, miR-483-5p and miR-629, were found to be potentially abnormally expressed in SLE T cells. After validation, under-expressed miR-145 and over-expressed miR-224 were noted. We further found that STAT1 mRNA targeted by miR-145 was over-expressed and apoptosis inhibitory protein 5 (API5) mRNA targeted by miR-224 was under-expressed in SLE T cells. Transfection of Jurkat cells with miR-145 suppressed STAT1 and miR-224 transfection suppressed API5 protein expression. Over-expression of miR-224 facilitates activation-induced cell death in Jurkat cells. In the clinical setting, the increased transcript levels of STAT1 were associated significantly with lupus nephritis. In conclusion, we first demonstrated that miR-145 and miR-224 were expressed aberrantly in SLE T cells that modulated the protein expression of their target genes, STAT1 and API5, respectively. These miRNA aberrations accelerated T cell activation-induced cell death by suppressing API5 expression and associated with lupus nephritis by enhancing signal transducer and activator of transcription-1 (STAT)-1 expression in patients with SLE.
Authors:
M-C Lu; N-S Lai; H-C Chen; H-C Yu; K-Y Huang; C-H Tung; H-B Huang; C-L Yu
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Clinical and experimental immunology     Volume:  171     ISSN:  1365-2249     ISO Abbreviation:  Clin. Exp. Immunol.     Publication Date:  2013 Jan 
Date Detail:
Created Date:  2012-12-03     Completed Date:  2013-02-19     Revised Date:  2014-01-10    
Medline Journal Info:
Nlm Unique ID:  0057202     Medline TA:  Clin Exp Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  91-9     Citation Subset:  IM    
Copyright Information:
© 2012 The Authors Clinical and Experimental Immunology © 2012 British Society for Immunology.
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MeSH Terms
Descriptor/Qualifier:
Adult
Apoptosis / genetics
Apoptosis Regulatory Proteins / biosynthesis
Female
Humans
Jurkat Cells
Lupus Erythematosus, Systemic / immunology*
Male
MicroRNAs / biosynthesis*,  genetics
Middle Aged
Nuclear Proteins / biosynthesis
STAT1 Transcription Factor / biosynthesis
T-Lymphocytes / immunology*
Transcriptome
Transfection
Chemical
Reg. No./Substance:
0/API5 protein, human; 0/Apoptosis Regulatory Proteins; 0/MIRN145 microRNA, human; 0/MIRN224 microRNA, human; 0/MicroRNAs; 0/Nuclear Proteins; 0/STAT1 Transcription Factor; 0/STAT1 protein, human
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