A functional microRNA binding site variant in IL-23R gene in systemic lupus erythematosus and rheumatoid arthritis: is there any correlation?

Alesaeidi, Samira; Dizghandi, Saeed Esmaeili; Siri, Goli; Mosallaei, Meysam; Kenarangi, Taiebe; Ghorashi, Tahereh; Soosanabadi, Mohsen

doi:10.1007/s11033-022-07922-z

Cited by 2 publications

(2 citation statements)

References 48 publications

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“…2 Basically, SLE emanates from uncontrolled auto-antibodies production against self-antigens comprising of DNA, nucleosomes, and histones and subsequent inflammation owing to the deposition of immune complexes. 3 The prevalence of SLE varies in different geographical areas ranging from 20 to 150 cases per 100,000 persons annually. 4 It has been reported that the prevalence of this disorder in Iran as a middle-east country is around 40 per 100,000 individuals.…”

Section: Introductionmentioning

confidence: 99%

Significant hypomethylation of MMP9 gene promoter in patients with systemic lupus erythematosus

Ehtesham

Mosallaei

Mahdiabadi

et al. 2023

Lupus

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Objective Scholars are exploring novel diagnostic and prognostic biomarkers with higher sensitivity and specificity for systemic lupus erythematosus (SLE). In this regard, DNA methylation alterations have aroused attention. The association between the dysfunction of MMP9 and TNFAIP3 genes and SLE has been previously demonstrated. Therefore, in this study, we investigated the methylation level of MMP9 and TNFAIP3 promoters in peripheral blood mononuclear cells (PBMCs) of SLE patients and healthy controls. Methods Eighty Iranian SLE patients and 77 healthy individuals were enrolled. The methylation quantification endonuclease-resistant DNA (MethyQESD) method was used to assess methylation levels of MMP9 and TNFAIP3 in extracted DNA of PBMCs. To quantify the diagnostic utility of the promoter methylation level of these genes, the receiver operating characteristic (ROC) curve was constructed. Results MMP9 promoter was significantly hypomethylated in SLE patients compared with healthy people ( p < 0.001), while there was no significant difference in terms of TNFAIP3 promoter methylation levels ( p = 0.167). Also, this differential MMP9 methylation was observed in patients with renal involvement and patients without renal involvement (42.07 ± 25.73 vs 56.74 ± 29.71, p = 0.007). ROC analyses indicated that the diagnostic power of the MMP9 promoter methylation level for SLE was 0.839 [95% CI (0.781–0.911)]. Moreover, MMP9 methylation level was negatively correlated with creatinine and anti-dsDNA concentration and positively correlated with C3 and C4 levels. Conclusion The results of this study highlight the application of MMP9 methylation level in PBMCs of SLE patients as a diagnostic biomarker.

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Section: Introductionmentioning

confidence: 99%

Significant hypomethylation of MMP9 gene promoter in patients with systemic lupus erythematosus

Ehtesham

Mosallaei

Mahdiabadi

et al. 2023

Lupus

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“…El análisis de cómo estos factores desencadenan una respuesta autoinmunitaria, relacionada con el inicio de la artritis reumatoide, ha derivado en un modelo preclínico que involucra al fenotipo de artritis reumatoide seropositiva, caracterizada por la elevación de biomarcadores, como el factor reumatoide y/o anticuerpos anti-péptido cíclico citrulinado, en fases previas a la enfermedad. Así, se sugiere que la interacción de los genes y el exposoma [11] [12] podrían interactuar en un período previo a la aparición de los primeros síntomas articulares. No obstante, este modelo no es equiparable para los fenotipos seronegativos [13].…”

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Effect of epigenetics on rheumatoid arthritis

Rada¹,

Mestre²,

Morales³

2023

Medwave

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Rheumatoid arthritis is an autoimmune and inflammatory disease that predominantly affects the diarthrodial joints. In this pathology, environmental or behavioral factors can act in synergy with genetic predisposition, accelerating the onset and severity of the disease. This link between the environment and the genome is mediated by epigenetic marks on deoxyribonucleic acid, including its methylation, histone modification, and noncoding ribonucleic acid-mediated regulation. Epigenetics can generate heritable phenotypic changes, which are not determined by modifications in the deoxyribonucleic acid sequence and are therefore reversible. Therefore, diet, medications and other environmental factors would have the ability to modulate them. The identification of a specific epigenetic dysregulation can offer a better understanding of the pathophysiology of the disease and positively influence the prevention, diagnosis and development of new therapeutic targets. Rheumatoid arthritis is an autoimmune and inflammatory disease that predominantly affects the diarthrodial joints. In this pathology, environmental or behavioral factors can act in synergy with genetic predisposition, accelerating the onset and severity of the disease. This link between the environment and the genome is mediated by epigenetic marks on deoxyribonucleic acid, including its methylation, histone modification, and noncoding ribonucleic acid-mediated regulation. Epigenetics can generate heritable phenotypic changes, which are not determined by modifications in the deoxyribonucleic acid sequence and are therefore reversible. Therefore, diet, medications and other environmental factors would have the ability to modulate them. The identification of a specific epigenetic dysregulation can offer a better understanding of the pathophysiology of the disease and positively influence the prevention, diagnosis and development of new therapeutic targets.

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A functional microRNA binding site variant in IL-23R gene in systemic lupus erythematosus and rheumatoid arthritis: is there any correlation?

Cited by 2 publications

References 48 publications

Significant hypomethylation of MMP9 gene promoter in patients with systemic lupus erythematosus

Significant hypomethylation of MMP9 gene promoter in patients with systemic lupus erythematosus

Effect of epigenetics on rheumatoid arthritis

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