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Cell Journal، جلد ۱۶، شماره Suppl ۱، صفحات ۱۰۳-۱۰۳
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عنوان انگلیسی Ps-71: Decreased Promoter Methylation of Interleukin-10 Gene in Leukocytes of Multiple Sclerosis Subjects
چکیده انگلیسی مقاله Objective: Multiple sclerosis (MS) is a neurodegenerative autoimmune disease characterized by recurrent episodes of demyelination and axonal injury mediated primarily by CD4+ T-helper cells with a pro inflammatory Th1 phenotype, macrophages, and soluble mediators of inflammation. Calcitriol (1α, 25(OH)2-vitamin D3) binds to the vitamin D receptor (VDR) and regulates differentiation of the immune cells, and may therefore be useful in the treatment of autoimmune diseases as an immunomoderator drug. Vitamin D3 clinically used to moderate patient's symptoms. But in some patients no clinical improvement had been observed any more. Nowadays, scientists' attention is focused on epigenetic alteration such as differences in CpG dinucleotide methylation of some disorders like Arthritis Rheumatoid, Lupus Erythematous, different type of cancers and so. VDR binds to Vitamin D3 and RXR (Retinoic acid receptor) and this heterodimer binds to VDRE (VDR Element) upstream of target genes.The aim of the study was to investigate whether the vitamin D could affect epigenetic alteration of IL-10 promoter and increase its expression level in positive groups with positive response to Vit D3 therapy. Materials and Methods: We extracted DNA from 15 cases of two groups –which respond (positive) and doesn't respond to Vit D3- and converted it by ZymoResearch bisulfite conversion kit. Specific primers was designated for potential region of the IL-10 promoter to perform Methylation Specific High Resolution Melting analysis (MS-HRM). Results: Our analysis shown different patterns between two groups. Further, our data confirmed by DNA sequencing. Conclusion: Promoter hypomethylation in CpG dinucleotides can directly affect and increase the expression of IL-10, so we concluded that vitamin D treatment could have an impact on epigenetic mechanisms of gene regulation.
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نشانی اینترنتی http://celljournal.org/journal/article/abstract/397
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