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Dr. Seham Gouda Amin Hassan Ali :: Publications:

Title:
MiR-155 expression is a potential biomarker of systemic lupus erythematosus diagnosis and disease activity prediction
Authors: Osama S. El-Shaera, Jehan H. Sabrya, Marwa Y. Mahgoubb, Nehal A. Hamedc,⁎, Dalia M. Nour El Dina, Seham G. Ameena
Year: 2020
Keywords: Keywords: MicroRNAs Systemic lupus erythematosus miR-155 Disease activity
Journal: Meta Gene,
Volume: 26
Issue: Not Available
Pages: Not Available
Publisher: Not Available
Local/International: International
Paper Link: Not Available
Full paper Seham Gouda Amin Hassan Ali_MiR-155 expression is a potential biomarker of systemic lupus.pdf
Supplementary materials Not Available
Abstract:

Background: Early diagnosis of Systemic Lupus Erythematosus (SLE) and its activity has a curtail role in the proper management of the disease with positive effect on its prognosis. MicroRNAs (miRNAs) evidently take apart in the pathogenesis of autoimmune diseases. Many miRNAs play a role in SLE pathogenesis and miR-155 is one of them. Objective: To examine miR-155 expression in patients with SLE and evaluate its role in the disease development and activity. Subjects and methods: The current study evaluated miR-155 expression in 60 SLE patients and 40 apparently healthy controls (HCs) using real-time polymerase chain reaction. Diagnosis was according to Systemic Lupus International Collaborating Clinics (SLICC) criteria. Disease activity was evaluated by systemic lupus erythematosus disease activity index (SLEDAI-2 K) score. Results: miR-155 level was significantly higher in SLE patients than controls with significant positive correlation with SLEDAI score and positive relation to renal involvement, proteinuria, pulmonary complications, fever and dsDNA antibodies. Multivariate regression analysis revealed that miR-155 is a significant risk factor for SLE. Conclusion: Overexpression of miR-155 occurs in SLE and it can be used as a predictor biomarker for disease's development and activity. It also may be a risk for renal involvement in the disease course. 1. Introduction Systemic Lupus Erythematosus (SLE) is a chronic autoimmune condition that is characterized by immunological tolerance lost and the development of pathogenic autoantibodies contributing to destruction of multiple organ systems with variable degree of severity (Fang and Orr-Skirvin, 2019). The immunopathogenesis of SLE is unclear, however the complex relationship between genetic, epigenetic, hormonal and environmental factors are predisposing factors (Momtaz et al., 2019). The missing connection between hereditary and environmental risk factors can be epigenetic pathways. Epigenetics relate to gene expression variations inherited by factors other than modifications to the standard DNA series. They involve DNA methylation, post-translation histone modifications and microRNA regulation (Richardson and Patel, 2014). MicroRNAs (miRNAs) are small, uniformly stranded, non-coding RNAs with a length from 18 to 25 nucleotides, behaving as a posttranscription negative gene expression regulator, by attaching to the target messenger RNAs (mRNAs), thereby preventing their translation into proteins or causing their degradation (Shumnalieva et al., 2018). Changes to the miRNA regulation are involved in cancer, degenerative, metabolic and autoimmune diseases such as SLE (Chen et al., 2017). Dysregulated miRNAs can assist SLE pathogenesis by managing interferon pathway type I, inflammatory cytokine production, T cell DNA methylation, and local tissue inflammation. In addition, miRNAs can affect the activity and intensity of the disease (Pérez-Sánchez et al., 2016). Most miRNAs come from blood cells and are balanced in tissues, plasma, serum and other body fluids, which promote their usage as biomarkers for SLE diagnosis, disease activity evaluation and therapeutic effectiveness assessment (Husakova, 2016). The existence of high sensitivity and low complex polymerase chain reaction (PCR) detection methods opposed to protein biomarkers is one of the main benefits of utilizing miRNAs as biomarkers for disease. In fact, early SLE https://doi.org/10.1016/j.mgene.2020.100770 Received 26 May 2020; Received in revised form 7 July 2020; Accepted 20 July 2020 ⁎ Corresponding author. E-mail address: neno.lab88@gmail.com (N.A. Hamed). Meta Gene 26 (2020) 100770 Available online 24 July 2020 2214-5400/ © 2020 Elsevier B.V. All rights reserved. T

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