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Niemann-Pick Disease, Type Ci Gene Expression in Pbmcs Is Associated With Interleukin 10 Serum Concentration: A Case-Control Study Publisher Pubmed



Zali F1 ; Teimouri M1 ; Shabani P1 ; Vatannejad A1 ; Najafi M2 ; Shateri H1 ; Asadnia M1 ; Doosti M1
Authors
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Authors Affiliations
  1. 1. Department of Clinical Biochemistry, School of Medicine, Tehran University of Medical Sciences (TUMS), Tehran, Iran
  2. 2. Tehran Heart Center, Tehran University of Medical Sciences, Tehran, Iran

Source: Clinical Laboratory Published:2018


Abstract

Background: Recent studies showed that atherosclerosis is a lysosomal storage disease (LSD) and Niemann-Pick disease type CI (NPC1) is the most important protein of the lysosomal membrane that is involved in the removal of FC from lysosomes. Whereas several in vitro and in vivo studies have described the crosstalk between lysosomal cholesterol accumulation and increased inflammation, there is no study addressing the correlation between NPC1 gene expression and an anti-inflammatory cytokine, interleukin 10 (IL-10) serum concentration in atherosclerotic patients. Methods: IL-10 and 25-hydroxyvitamin D serum concentrations were quantified by enzyme-linked immunosorbent assay (ELISA) in atherosclerotic patients (n = 40) and a control group (n = 40). NPC1 gene expression analysis was performed by quantitative real-time PCR, and correlation between the two parameters was assessed. Results: Mean IL-10 serum concentration and peripheral blood mononuclear cells' (PBMCs) gene expression of NPC1, adjusted for drug consumption, age, and BMI, was not significantly different between the patient and control groups (p = 0.6 and 0.67 respectively). However, NPC1 gene expression showed positive significant correlation with IL-10 serum concentration (p = 0.04, r = 0.29). We also observed lower serum concentration of IL-10 in the subjects with lower 25-hydroxyvitamin D serum concentration (p = 0.034). Conclusions: Our findings supported the previous observations showing the contribution of lysosomal lipid homeostasis of PBMCs to inflammation and pathogenesis of atherosclerosis. © 2018 Verlag Klinisches Labor GmbH. All rights reserved.