Evaluation of Survivin Expression and Regulating Mirnas of Survivin Expression in Peripheral Blood Mononuclear Cells in Systemic Lupus Erythematous Patients Publisher Pubmed



Bolouri N^{1, 2} ; Mansouri R¹ ; Farhadi E^{2, 3} ; Soltani S² ; Akhtari M⁴ ; Madreseh E^{2, 3} ; Faezi ST² ; Jafarinejadfarsangi S⁵ ; Jamshidi A² ; Mahmoudi M^{2, 3} Show Affiliations
Source: Lupus Published:2024

Abstract

Background: Systemic lupus erythematosus is a multisystemic rheumatic disease with different clinical features. Disturbance in apoptosis regulation seems to be a major factor in SLE development. Objective: Survivin plays a key role in mitosis and inhibiting apoptosis. A study was conducted to examine the expression level of survivin and miRNAs that affect survivin transcript levels in patients with SLE. Methods: We isolated peripheral blood mononuclear cells from 50 inactive SLE patients and 50 healthy controls. RNA is extracted and converted to cDNA. The quantitative real‐time polymerase chain reaction is conducted to assess the expression levels of survivin total and its variants with effective miRNAs in PBMCs. Results: Expression levels of miR-34a-5p (fold change = 1.5, p++ = 0.027), and 218-5p (fold change = 1.5, p++ = 0.020) were significantly increased. While miR-150-5p (fold change = 0.56, p++ = 0.003) was significantly decreased. The mRNA expression of survivin-WT (fold change = 0.63, p++ = 0.002) was significantly downregulated in SLE patients compared to the healthy controls. Survivin total and its two major variants (survivin-2B, and survivin-ΔEx3) did not differ significantly between SLE patients and controls. Conclusion: Although survivin-TS and its two variants (survivin-2B, and survivin-ΔEx3) were not differently expressed in SLE patients, survivin-WT had altered expression. Despite aberrant miRNA expression in PBMCs from SLE patients, survivin and miRNA expression were not associated with leukopenia. The pathogenesis of SLE disorder might be linked to survivin’s other roles in the immune system aside from anti-apoptotic functions. © The Author(s) 2024.