Association Between Cox-2 and 15-Pgdh Polymorphisms and Sle Susceptibility Publisher Pubmed



Sandoughi M¹ ; Saravani M^{2, 3} ; Rokni M^{4, 5} ; Nora M² ; Mehrabani M⁶ ; Dehghan A⁷
Source: International Journal of Rheumatic Diseases Published:2020

Abstract

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. © 2020 Asia Pacific League of Associations for Rheumatology and John Wiley & Sons Australia, Ltd