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Research Articles

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

, ORCID Icon, , , , , , , & show all
Pages 515-519 | Received 28 Mar 2022, Accepted 14 Aug 2022, Published online: 29 Sep 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.

Acknowledgment

We would like to thank patients and control individuals for their participation.

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

Funding information this work was supported by the following Brazilian funding agencies: CAPES (Coordination for the Improvement of Higher Education Personnel), CNPq (Conselho Nacional in Scientific and Technological Development) and FACEPE (Fundação de Amparo à Ciência e Tecnologia de Pernambuco).

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