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جستجوی مقالات
یکشنبه 23 آذر 1404
Cell Journal
، جلد ۱۶، شماره Suppl ۱، صفحات ۱۰۲-۱۰۲
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عنوان انگلیسی
Ps-70: Epigenetic Alteration by DNA Promoter Hypermethylation of Vitamin D Receptor in Multiple Sclerosis Patients
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 determine whether is the VDR promoter methylation cause of its low expression in those group that doesn't respond to Vitamin D3 therapy or not.Materials and Methods: We used bisulfite converted DNA, which extracted from 15 cases of two groups –which respond and doesn't respond to Vitamin D3- and converted by ZymoResearch bisulfite conversion kit, and specific primers for three potential regions of the VDR CpG island 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 hypermethylation in CpG dinucleotides can directly affect and reduce the expression of VDR, so we concluded that vitamin D treatment could have an impact on epigenetic mechanisms of gene regulation.
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http://celljournal.org/journal/article/abstract/396
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