Mohammad Taher Tahoori, Ali Akbar Pourfathollah, Saeed Daneshmandi, Masoomeh Akhlaghi,
Volume 14, Issue 6 (1-2012)
Abstract
Background: Programmed death 1 (PDCD1), a negative T-cell regulator which induces peripheral tolerance, belongs to Ig super and CD28/CTLA-4 families. PD-1 gene induces negative signals in T-cells during interaction with its ligands. Thus the aim of this study was to investigate the relationship between PD-1 polymorphism and the risk of rheumatoid arthritis (RA) in Iranian patients and healthy controls.
Materials and Methods: In this case-control study, genomic DNA was extracted from the whole blood samples using DNA purification kit (DNG-plus, Cinnagen, Iran). PD1.1G/A as a SNP located on promoter with position -536 were genotyped for 120 RA patients and 188 healthy controls through PCR-RFLP method. Association of genotypes and alleles frequency in the patients was compared with controls and analyzed using Chi-square test and 2×2 contingency table in SPSS software version 15.0. The diagnosis of RA patients and provision of their clinical information was done in Rheumatology Research Center of Tehran University of Medical Sciences, Tehran, Iran.
Results: The A allele of the PD1.1 polymorphism located on the promoter of PD-1 gene was significantly more frequent in Iranian RA patients than the controls (p=0.04). There were no significant differences in PD1.1G/G genotype (p=0.08), PD1.1A/A genotype (p=0.39), and PD1.1G/A genotype (p=0.16) between RA cases and controls.
Conclusion: The findings of this study showed the presence of a significant relationship between the A allele of the PD1.1 (-536) of the promoter and susceptibility to RA in Iranian patients.
Nahideh Talebzadeh, Saeid Ghorbian,
Volume 21, Issue 4 (8-2018)
Abstract
Background and Aim: Metabolic syndrome (MS) was committed multiple disorders including diabetes, hypertension, and obesity, which were played influential effects on the mortality rates of patients suffering from of cardiovascular disorders. Vascular endothelial growth factor (VEGF) is a protein that stimulates vascular and angiogenesis. One of the most common epigenetic changes is methylation of the promoter regions of genes, which leads to the regulation of gene expression. We aimed to assess the methylation pattern of promoter regions of VEGF gene which may act a critical role in the pathogenesis of MS.
Materials and Methods: In this descriptive-analytical investigation, we have assessed a total of 100 subjects, which were included 50 of cases diagnosed as MS and 50 healthy individuals as a control group. Methyl specific polymerase chain reaction (MS–PCR) method was performed to analyzing of VEGF gene promoter methylatin patterns and data analysis was performed using Chi Square test and SPSS 23 software.
Findings: The frequencies of VEGF gene promoter methylation observed in 32% and 20% of case and control individuals, respectively. Our findings revealed that the frequencies of the gene methylated were not statistically different between two groups (p=0.239). In other hand, our findings revealed a statistically significant difference regarding to the clinical parametrics including, triglycired (p=0.050), cholesterol (p=0.046), suger blood (p=0.025) and HbA1C (p=0.016) between cases and control groups (p=0.05).
Conclusion: According to our findings, methylation alteration in VEGF gene did not show any critical role in the pathogenesis of MS and it is suggested that more evidence will be needed to approve the present results.
