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Circulating Levels of Il-35 and Gene Expression of Foxp3 in Coronary Artery Disease: Is There Any Interplay Between Them and 25-Hydroxyvitamin D3? Publisher Pubmed



Shateri H1 ; Fadaei R1 ; Najafi M2 ; Vatannejad A1 ; Teimouri M1 ; Zali F1 ; Emamgholipour S1 ; Parvaz E3 ; Asadnia M1 ; Doosti M1
Authors
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Authors Affiliations
  1. 1. Department of Biochemistry, Faculty of Medicine, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran
  3. 3. Department of Clinical Biochemistry, Faculty of Medicine, Tarbiat Modarres University, Tehran, Iran

Source: Clinical Laboratory Published:2018


Abstract

Background: We aimed to evaluate interleukin-35 (IL-35) serum levels and the forkhead box P3 (FoxP3) expression in peripheral blood mononuclear cells (PBMCs) of coronary artery disease (CAD) patients compared with the non-CAD group. Also, we examined the possible relationship between gene expression of FoxP3 and serum levels of IL-35 with several CAD-related clinical parameters. Methods: This study was conducted on 40 men with CAD and 40 men with a normal coronary artery. The gene expression of FoxP3 was measured by real-time polymerase chain reaction (real-time PCR). The serum concentrations of IL-35 and 25-hydroxyvitamin D3 (25(OH)D3) were measured by enzyme-linked immunosorbent assay (ELISA). Results: FoxP3 gene expression was significantly decreased in patients compared to controls (p = 0.01). Serum concentrations of IL-35 and 25(OH)D3 were significantly reduced in patients in comparison with the control group (both, p < 0.001), and reduction of IL-35 showed an independent association with CAD. IL-35 levels had a significant positive correlation with serum 25(OH)D3 (r = 0.266, p = 0.044) in the whole population. Moreover, there was an inverse correlation between the FoxP3 expression and CAD severity in CAD patients (r = -0.372, p = 0.01). Conclusions: It appears that reduced mRNA expression of FoxP3 and circulating level of IL-35 are of significance in the context of CAD pathogenesis. However, more studies are required to elucidate underlying mechanisms. © 2018 Verlag Klinisches Labor GmbH. All rights reserved.
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