Abstract
Background: Comprised of two main subtypes (Ulcerative Colitis (UC) and Crohn), inflammatory bowel disease is caused by an interaction between genetic and environmental factors. As of the important role of innate immunity and JAK/STAT signaling pathway, the current study was designed to investigate the methylation status JAK2 gene in blood and tissue samples of patients with UC.
 Methods: Genomic DNA was extracted from blood and intestinal biopsy samples of 28 UC patients and 28 controls. After bisulfite DNA conversion, real-time quantitative multiplex methylation specific PCR (QM-MSP) method was applied in order to assess JAK2 promotor methylation status.
 Results: The JAK2 promotor in the intestinal biopsy samples was significantly hypermethylated in UC as the mean of unmethylated DNA was 1.255±1.865 in the patients group, while it was 1.292±4.726 in control group.
 Conclusion: Hypermathylation of JAK2 gene may play a part in pathophysiology of UC which could result in gene silencing.
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