Long Noncoding RNAs in the Regulation of Inflammatory Pathways of MS

سال انتشار: 1397
محل انتشار: سومین کنگره بین المللی و پانزدهمین کنگره ملی ژنتیک ایران
کد COI اختصاصی: CIGS15_358
زبان مقاله: انگلیسی
تعداد مشاهده: 337

نویسندگان

Department of cellular and molecular biology, Shahid Beheshti University, Tehran, Iran

چکیده

Background: Multiple sclerosis (MS) is a chronic autoimmune, inflammatory neurological disease of the central nervous system (CNS).[1] As the pathophysiologic and pharmacological indicators, studies on biomarkers in MS are useful for early prediction and diagnosis, monitoring of disease activity and predicting treatment response.[2] Long non-coding RNAs (lncRNAs) have been recently reported to participate in the regulation of immune responses.[3] In multiple sclerosis (MS), NF-kB pathways are changed, leading to increased levels of NF-kB activation in cells. This may indicate a key role for NF-kB in MS pathogenesis.[4]Liu et al. found that NKILA (1) is upregulated by immunostimulants, (2) has a promoter with an NF-ĸB binding motif, (3) can bind to the p65 protein of the NF-ĸB transcription factor and then interfere with phosphorylation of IĸBα, and (4) negatively affects functions that involve NF-ĸB pathways.[5] Methods: We examined expression levels of NKILA in 40 patients with MS and 33 healthy subjects. The expression level of NKILA was examined by qRT-PCRResults: The expression of NKILA was up-regulated in MS patients. Moreover, we found some significant correlations between lncRNA expression levels and clinical data of MS patients.Conclusion: Our results shed further light to the inflammatory aspects of MS with emphasis to the regulatory role of this lncRNA in the physiopathology of MS. NF-KappaB Interacting LncRNA (NKILA), which is upregulated by NF-kB, binds to NF-kB/IkB, and directly masks phosphorylation motifs of IkB, thereby inhibiting IKK-induced IkB phosphorylation and NF-kB activation.

کلیدواژه ها

multiple sclerosis; long noncoding RNAs; biomarkers; NF-kB; NKILA

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