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Association of Intrinsic and Induced Genomic Instability in Peripheral Blood Lymphocytes of Type 2 Diabetes Patients With Expression Level of Genes Prkcb and Sp1) and Micrornas (Mir-126 and Mir-15A-3P) Publisher



Samanian S1 ; Mozdarani H1 ; Behmanesh M2 ; Nasliesfahani E3
Authors
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Authors Affiliations
  1. 1. Department of Medical Genetics, Faculty of Medical Sciences, Tarbiat Modares University, Tehran, Iran
  2. 2. Department of Genetics, Faculty of Biological Sciences, Tarbiat Modares University, Tehran, Iran
  3. 3. Diabetes Research Center, Endocrinology and Metabolism Clinical Science Institute, Tehran University of Medical Sciences, Tehran, Iran

Source: Acta Medica Mediterranea Published:2019


Abstract

Background: Type 2 diabetes mellitus (T2D) is a metabolic disorder that its prevalence has been increasing all over the world so the number of people affected expected to double in the next decade. In this study we aim to investigate the expression level of genes (SP1 and PRKCB) and microRNAs (miR-126 and miR-15a-3p) and genomic instability in T2D patients. Methods: Blood samples from 20 Iranian T2D patients and 20 Iranian normal individuals during 2016-2017 were obtained for measuring the expression level of SP1, PRKCB, miR-126 and miR-15a-3p by Real time RT-PCR and evaluating genomic instability by G2 assay technique. Statistical analyses were performed with the SPSS software ver. 23 and P values <0.05 was considered as statistically significant. The Kolmogorov-smirnov test, Independent-Samples t-test, One Way ANOVA and correlation test were used. Results: The expression level of the SP1 and PRKCB genes showed a significant increase in T2D patients compared to normal individuals, miR-126 and miR-15a-3p showed a significant decrease in T2D patients compared to normal individuals Furthermore, the genomic instability was correlated with expression level of these genes and microRNAs. Conclusions: Our study shows that these genes and microRNAs are involved in genomic instability of T2D and may be also involved in the pathogenesis of T2D. © 2019 A. CARBONE Editore. All Rights Reserved.