Hypomethylation of OAS2 and OAS3 Gene Promoters: Insights into the ‎Pathogenesis of Systemic Lupus Erythematosus

DNA methylation plays a key role in systemic lupus erythematosus (SLE) by regulating gene expression and impacting immune system functions. In SLE, abnormal DNA methylation patterns can lead to the overexpression of pro-inflammatory genes and downregulation of the regulatory genes, contributing to a...

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Vydáno v:Iranian journal of immunology Ročník 22; číslo 2; s. 155
Hlavní autoři: Rigi Yousefabadi, Esmat, Ourang, Zahra, Gharibdoost, Farhad, Faezi, Seyedeh Tahereh, Saatchi, Mohammad, Gholami, Delnya, Esmaeilzadeh, Emran, Khorram Khorshid, Hamid Reza
Médium: Journal Article
Jazyk:angličtina
Vydáno: Iran Shiraz Institute for Cancer Research 23.06.2025
Témata:
Autoimmunity
Creatinine
DNA methylation
Endonuclease
Gene expression
Genes
Immune system
Leukocytes (mononuclear)
Lupus
Peripheral blood mononuclear cells
Systemic lupus erythematosus
Systemic lupus erythematosus
Methylation
OAS2
OAS3
ISSN:1735-1383, 1735-367X, 1735-367X
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Shrnutí:DNA methylation plays a key role in systemic lupus erythematosus (SLE) by regulating gene expression and impacting immune system functions. In SLE, abnormal DNA methylation patterns can lead to the overexpression of pro-inflammatory genes and downregulation of the regulatory genes, contributing to autoimmunity. This dysregulation can increase susceptibility to SLE. Understanding these methylation changes could help discover new therapeutic strategies for managing SLE. To evaluate methylation levels of OAS2 and OAS3 in peripheral blood mononuclear cells (PBMCs) in volunteers with SLE were evaluated. In this case-control study, we collected 207 peripheral blood samples from 102 SLE patients and 105 healthy subjects. After isolating the PBMCs, methylation analysis was performed using the methylation-quantification of endonuclease-resistant DNA (MethyQESD) method. The control group had an average OAS2 methylation percentage of 40.02% ± 24.59%, whereas the SLE group had a significantly lower average of 19.46% ± 21.98%. This finding indicates a significant hypomethylation of OAS2 in the SLE cohort (P<0.001). Additionally, a significant difference was observed in the mean methylation levels of OAS3, with SLE patients exhibiting 14.11% ± 19.50% compared to healthy controls at 25.32% ± 20.82% (P<0.001). Patients with renal damage also showed significantly lower OAS2 methylation levels than SLE individuals without renal damage (P<0.001). Furthermore, a negative connection was found between the OAS2 methylation level and creatinine (r= -0.266, P= 0.007). The pattern of methylation levels observed in OAS2 and OAS3 within PBMCs may provide valuable insights into the mechanisms underlying SLE development.
Bibliografie:ObjectType-Article-1
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ISSN:1735-1383
1735-367X
1735-367X
DOI:10.22034/iji.2025.105409.2944