Author/Authors :
Sanati, Golshid Department of Immunology - School of Medicine - Tehran University of Medical Sciences, Tehran, Iran , Jafari, Davood Department of Immunology - School of Medicine - Zanjan University of Medical Sciences, Zanjan, Iran - Immunogenetics Research Network (IgReN) - Universal Scientific Education and Research Network (USERN), Zanjan, Iran , Noruzinia, Mehrdad Department of Medical Genetics - Faculty of Medical Sciences - Tarbiat Modares University, Tehran, Iran , Ebrahimi Daryani, Naser Department of Internal Medicine - Division of Gastroenterology - Imam Khomeini Hospital - Tehran University of Medical Sciences, Tehran, Iran , Ahmadvand, Mohammad Department of Medical Genetics - Faculty of Medical Sciences - Tarbiat Modares University, Tehran, Iran , Teimourian, Shahram Department of Genetics - School of Medicine - Iran University of Medical Sciences, Tehran, Iran , Rezaei, Nima Research Center for Immunodeficiencies - Children's Medical Center - Tehran University of Medical Sciences, Tehran, Iran - Network of Immunity in Infection - Malignancy and Autoimmunity (NIIMA) - Universal Scientific Education and Research Network (USERN), Boston, MA, USA
Abstract :
Background: Growing evidence supports that changes in the methylation state of In-flammatory Bowel Disease (IBD)-associated genes could significantly alter levels of gene expression, potentially contributing to disease onset and progression. We sup-posed that alterations in DNA methylation status at promoter region within the sup-pressor of cytokine signaling 3 (SOCS3) gene in intestinal tissues may be involved in the susceptibility to Crohn's Disease (CD).
Methods: DNA methylation status in the promoter region of the human SOCS3 gene of intestinal tissues from 15 patients with CD and 15 age- and sex-matched healthy controls were profiled using the real-time Quantitative Multiplex Methylation Specific PCR (QM-MSP) assay.
Results: Based on methylation assay data profiling, we found that patients with CD showed a higher degree of methylation of the SOCS3 gene promoter region than did the healthy controls (unmethylated DNA in CD vs. healthy controls; 0.00048±0.0011 vs. 0.07±0.142, p<0.000).
Conclusion: The data presented here demonstrate that aberrant methylation of the CpG islands within promoter regions of SOCS3 gene in colonic mucosa of CD was asso-ciated with mucosal inflammatory status, providing insights into the involvement of methylation could contribute to the initiation of the inflammatory process and devel-opment of CD.
Keywords :
Crohn's disease , DNA methylation , Epigenetics , Immune regulation , SOCS3
