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Serum miRNA-122 expression in non-alcoholic fatty liver disease among Egyptian patients and its correlation with interleukin-1A gene polymorphism
Update time:2017-08-16 10:57:00   【 Font: Large  Medium Small

Abstract

MicroRNAs (miRNAs) are of interest because they are dysregulated in different diseases, including liver diseases. MicroRNA-122 is an organ specific miRNA representing 70% of total miRNA in hepatocytes. The aim of this study was to investigate serum miRNA-122 expression in Egyptian patients with non-alcoholic fatty liver disease (NAFLD) and to determine its relationship with insertion/deletion polymorphism within the 3′ UTRs regions of interleukin-1A (IL-1A) gene which represents the binding site of miRNA-122. The study included 75 healthy subjects and 75 patients with NAFLD. Patients were recruited from the internal medicine outpatient clinic at Suez Canal University Hospital, Ismailia, Egypt. Serum miRNA-122 expression was determined using quantitative real-time PCR and normalization was done against RNU6B as an internal control. Our results reveled that about 76% of patients exhibited up-regulation of miRNA-122. The median miRNA-122 expression level in patients increased significantly (6.68 fold) compared to control (p = 0.001). Serum miRNA-122 expression level in NAFLD patients showed positive correlation with both serum triglycerides (TG) and very low density lipoprotein-cholesterol (VLDL-C) level (p = 0.048), and with serum IL-1A (p = 0.03). Regarding the relation between serum miRNA-122 expression and different genotypes of IL-1A insertion/deletion gene polymorphism (DD, ID, and II genotypes), patients carrying the major high risk DD genotype had a significant increase in miRNA-122 expression than those with heterozygous ID and the homozygous II genotypes (p = 0.002). In conclusion, serum miRNA-122 expression showed positive association with increased susceptibility to NAFLD in the study population. Insertion/deletion IL-1A gene polymorphism may be a marker for genetic susceptibility to NAFLD in Egyptian population, likely through miRNA-122 mediated regulation.


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