HOTAIR but not ANRIL long non‐coding RNA contributes to the pathogenesis of multiple sclerosis. Issue 4 (16th November 2017)

• Record Type: Journal Article
• Authors: Pahlevan Kakhki, Majid; Nikravesh, Abbas; Shirvani Farsani, Zeinab; Sahraian, Mohammad Ali; Behmanesh, Mehrdad
• Is Part Of: Immunology. Volume 153:Issue 4(2018)
• Page Start: 479
• Page End: 487
• Publication Date: 2017-11-16
• Subjects: ANRIL -- experimental autoimmune encephalomyelitis -- HOTAIR -- long non‐coding RNAs -- multiple sclerosis -- vitamin D; Immunology -- Periodicals
• DOI: 10.1111/imm.12850
• Languages: English
• ISSNs: 0019-2805

Abstract

Summary: Studies have revealed that dysregulation in gene expression is one of the main aspects of multiple sclerosis (MS) pathogenesis. Although the molecular pathways underlying the immunomodulatory role of vitamin D (VD) in MS is not completely elucidated, VD has more recently become a topic of interest in immune regulation and is widely administered to patients with MS as an immunomodulatory supplement. Long non‐coding RNAs (lncRNAs) are known to play important roles in regulation of gene expression via different mechanisms. Given that VD‐related genes are regulated by epigenetic mechanisms, here we aimed to evaluate the role of VD in combination with HOTAIR and ANRIL lncRNAs using in vivo, in vitro and in silico experiments in MS pathogenesis. Our data revealed that HOTAIR but not ANRIL lncRNA is probably involved in the pathogenesis of MS and experimental autoimmune encephalomyelitis through an unclear mechanism and it seems that by affecting the expression, inflammation and VD can influence HOTAIR ‐related mechanisms, which require further study. Abstract : The effect of vitamin D (VD) supplementation on the expression levels of human HOTAIR and ANRIL long non‐coding RNAs and VD receptor mRNA. We found a significant difference between the expression levels of HOTAIR (A, B) but not ANRIL (C, D) long non‐coding RNA before supplementation versus controls. Interestingly, the expression of VD receptor (E) significantly decreased before versus after supplementation.