Avicenna J Med Biotech

arij002

Avicenna Journal of Medical Biotechnology

2008-2835 2008-4625

Avicenna Research Institute

ajmb60499

Association of Aberrant Promoter Methylation Changes in the Suppressor of Cytokine Signaling 3 (SOCS3) Gene with Susceptibility to Crohn's Disease

Sanati

Golshid

Jafari

Davood

Noruzinia

Mehrdad

Research and Production plant, Pasteur Institute of Iran , Karaj, Iran

Ebrahimi-Daryani

Naser

Monoclonal Antibody Research Center, Avicenna Research Institute, ACECR , Tehran, IranDepartment of Immunology, School of Public Health, Tehran University of Medical Sciences , Tehran, Iran

Ahmadvand

Mohammad

Teimourian

Shahram

Rezaei

Nima

Biotechnology Department, Biotechnology Research Center, Pasteur Institute of Iran , Tehran, Iran

14 2 165 169 27 11 2021 30 1 2022

Background: Growing evidence supports that changes in the methylation state of Inflammatory Bowel Disease (IBD)-associated genes could significantly alter levels of gene expression, potentially contributing to disease onset and progression. We supposed that alterations in DNA methylation status at promoter region within the suppressor 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 associated with mucosal inflammatory status, providing insights into the involvement of methylation could contribute to the initiation of the inflammatory process and development of CD.