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Association between COX‐2 and 15‐PGDH polymorphisms and SLE susceptibility
Author(s) -
Sandoughi Mahnaz,
Saravani Mohsen,
Rokni Mohsen,
Nora Mehrangiz,
Mehrabani Mehrnaz,
Dehghan Azizallah
Publication year - 2020
Publication title -
international journal of rheumatic diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.795
H-Index - 41
eISSN - 1756-185X
pISSN - 1756-1841
DOI - 10.1111/1756-185x.13808
Subject(s) - genotyping , genotype , medicine , allele , single nucleotide polymorphism , immunology , odds ratio , genetics , biology , gene
Aims Systemic lupus erythematosus (SLE) is a chronic inflammatory autoimmune disease. Prostaglandins E2 (PGE2), the product of the cyclo‐oxygenase 2 (COX‐2) enzyme, has critical roles in the etiology of autoimmune diseases. PGE2 level is controlled by a balance between its synthesis mediator (COX‐2 enzyme) and its catabolic key enzyme (15‐hydroxyprostaglandin dehydrogenase [15‐PGDH] enzyme). In the present study, the associations of genotypic polymorphisms in COX‐2 and 15‐PGDH with SLE were investigated. Methods One hundred and sixty SLE patients and 160 healthy controls participated in the study. The polymerase chain reaction ‐ restriction fragments length polymorphism method was used for genotyping. The COX‐2 rs2745557 G/A and 15‐PGDH rs8752 G/A polymorphisms were investigated. Results Regarding the COX‐2 rs2745557 single nucleotide polymorphism, there was no significant association between COX‐2 rs2745557 polymorphism and SLE. However, the dominant models showed a marginally significant relation ( P = .048, odds ratio = 0.63, 95% CI = 0.4‐1.0). Regarding GA genotype of 15‐PGDH rd8752 polymorphism, there was a significant difference between two groups with a 4.5‐fold increase in SLE development ( P = .0001). The frequency of the A allele was higher in SLE patients than that in controls, showing a 1.4‐fold increase in SLE development ( P = .018). Conclusion All results showed the protective effects of the dominant model of COX‐2 rs2745557 polymorphism and risk factor of 15‐PGDH rs8752 polymorphism on SLE development.