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Expression of the miR-9-5p, miR-125b-5p and its target gene NFKB1 and TRAF6 in childhood-onset systemic lupus erythematosus (cSLE).

Authors :
Nascimento, Denise de Queiroga
da Silva, Isaura Isabelle Fonseca Gomes
Lima, Camilla Albertina Dantas
Cavalcanti, André de Souza
Roberti, Luciana Rodrigues
Queiroz, Rosane Gomes de Paula
Ferriani, Virginia Paes Leme
Crovella, Sergio
Carvalho, Luciana Martins de
Sandrin-Garcia, Paula
Source :
Autoimmunity. Dec2022, Vol. 55 Issue 8, p515-519. 5p.
Publication Year :
2022

Abstract

Childhood- onset systemic lupus erythematosus (cSLE) is a multisystem inflammatory disease that can lead to severe clinical conditions resulting in early comorbidities. Several genetic, environmental, and immunological factors are known to influence the onset of the disease. MiRNAs have been already considered as potential actors involved in the development and activity of the SLE. Thus, understanding the behavior of these regulators can contribute to clarify the inflammatory process affecting SLE patients. Among miRNAs, miR-125b-5p and miR-9-5p targeting NFKB1 and TRAF6 genes can be involved in the etio-pathogenesis of the disease by modulating inflammation. In this study we evaluated miR-9-5p and miR-125b-5p expression and its target genes NFKB1 and TRAF6 in peripheral blood samples (PBMC) from the 35 cSLE patients and 35 healthy controls. MiRNAs and gene target expression have been evaluated by using RT-PCR with specific TaqMan® probes. Both miR-9-5p [Fold Change (FC) = −2.21; p = 0.002] and miR-125b-5p (FC= −3.30; p < 0.0001) and NFKB1 (FC = −1.84; p < 0.001) were downregulated in cSLE patients, while TRAF6 was upregulated (FC = 1.80; p = 0.006) in cSLE patients when compared to controls. A significant correlation was found between miR-125b-5p and its target gene NFKB1 [Spearman (r) = 0.47; p = 0.023]. Our results showed miR-125b-5p and miR-9-5p differential expression in cSLE patients, possibly contributing to better understanding the role of these regulators in cSLE development and disease pathogenesis. [ABSTRACT FROM AUTHOR]

Details

Language :
English
ISSN :
08916934
Volume :
55
Issue :
8
Database :
Academic Search Index
Journal :
Autoimmunity
Publication Type :
Academic Journal
Accession number :
159687444
Full Text :
https://doi.org/10.1080/08916934.2022.2128781