miR-9-5p、miR-125b-5p及其靶基因NFKB1和TRAF6在儿童期系统性红斑狼疮(cSLE)中的表达

IF 3.3 4区 医学 Q3 IMMUNOLOGY Autoimmunity Pub Date : 2022-12-01 Epub Date: 2022-09-29 DOI:10.1080/08916934.2022.2128781
Denise de Queiroga Nascimento, Isaura Isabelle Fonseca Gomes da Silva, Camilla Albertina Dantas Lima, André de Souza Cavalcanti, Luciana Rodrigues Roberti, Rosane Gomes de Paula Queiroz, Virginia Paes Leme Ferriani, Sergio Crovella, Luciana Martins de Carvalho, Paula Sandrin-Garcia
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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]. 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引用次数: 5

摘要

儿童期全身性红斑狼疮(cSLE)是一种多系统炎症性疾病,可导致严重的临床症状,导致早期合并症。已知几种遗传、环境和免疫因素可影响该病的发病。mirna已经被认为是参与SLE发展和活动的潜在参与者。因此,了解这些调节因子的行为有助于阐明影响SLE患者的炎症过程。在mirna中,靶向NFKB1和TRAF6基因的miR-125b-5p和miR-9-5p可通过调节炎症参与疾病的发病机制。在这项研究中,我们评估了miR-9-5p和miR-125b-5p及其靶基因NFKB1和TRAF6在35名cSLE患者和35名健康对照的外周血样本(PBMC)中的表达。利用特异TaqMan®探针进行RT-PCR,评估mirna和基因靶表达。miR-9-5p [Fold Change (FC) = -2.21;p = 0.002]和miR-125b-5p (FC= -3.30;p NFKB1 (FC = -1.84;p TRAF6上调(FC = 1.80;p = 0.006)。miR-125b-5p与其靶基因NFKB1之间存在显著相关性[Spearman (r) = 0.47;p = 0.023]。我们的研究结果显示miR-125b-5p和miR-9-5p在cSLE患者中的差异表达,可能有助于更好地理解这些调节因子在cSLE发展和疾病发病机制中的作用。
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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).
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.
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来源期刊
Autoimmunity
Autoimmunity 医学-免疫学
CiteScore
5.70
自引率
8.60%
发文量
59
审稿时长
6-12 weeks
期刊介绍: Autoimmunity is an international, peer reviewed journal that publishes articles on cell and molecular immunology, immunogenetics, molecular biology and autoimmunity. Current understanding of immunity and autoimmunity is being furthered by the progress in new molecular sciences that has recently been little short of spectacular. In addition to the basic elements and mechanisms of the immune system, Autoimmunity is interested in the cellular and molecular processes associated with systemic lupus erythematosus, rheumatoid arthritis, Sjogren syndrome, type I diabetes, multiple sclerosis and other systemic and organ-specific autoimmune disorders. The journal reflects the immunology areas where scientific progress is most rapid. It is a valuable tool to basic and translational researchers in cell biology, genetics and molecular biology of immunity and autoimmunity.
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