Correlation between LincR-Gng2-5′and LincR-Epas1-3′as with the severity of multiple sclerosis in Egyptian patients

Abstract

Introduction: Multiple sclerosis (MS) is an immune-mediated disorder. Long noncoding RNAs (lncRNAs, LncR, Linc RNA) have role in many autoimmune and inflammatory disorders, including MS. LincR-Gng2-5 AS locus in T helper 1 cell (TH1) and LincR-Epas1-3AS in T helper 2 cell (TH2) cell were located in a genomic region rich in genes code for proteins with immune regulatory function. Our aim was to evaluate the LincR-Gng2-5′ and LincR-Epas1-3′AS fold change in blood of MS patients versus healthy controls and correlate it with disease severity, assessed based on Expanded Disability Status Scale (EDSS).

Material and Methods: Sixty MS patients 42 relapsing remitting (RR, RRMS), 18 Secondary progressive (SP, SPMS) and sixty controls (age-matched and sex-matched) were studied. Blood of patients and control group undergone the investigation of LincR-Gng2-5′ and LincR-Epas1-3′AS fold change by real-time PCR. Fold change >2 and p < .05 represent significant result.

Results: LincR-Gng2-5′ was significantly upregulated in MS patients with mean fold change (2.559) and (p = .03). Meanwhile, LincR-Epas1-3′AS levels were significantly downregulated with mean fold change (0.5964) and (p < .004). Patients with SP showed a significantly higher level of LincR-Gng2-5-fold change (3.71 ± 0.7) than that of RR (1.33 ± 0.3). LincR-Epas1-3′AS was markedly reduced among SP (0.43 ± 0.2) than that of RR (0.66 ± 0.1) but with no significant difference. As regards disease severity (EDSS); there was a significant positive correlation with LincR-Gng2-5 and negative correlation with LincR-Epas1-3′AS. LincR- Gng2-5and LincR-Epas1-3′AS, both are dysregulated in MS patient suggesting a role in disease pathogenesis.

Conclusion: LincR-Gng2-5 AS and LincR-Epas1-3′AS fold change are correlated to MS severity (EDSS).

Keywords:

• Multiple sclerosis
• long noncoding RNA
• LincR-Gng2-5′
• LincR-Epas1-3′AS

Acknowledgments

This study was performed at the Department of Medical Biochemistry and Molecular Biology Faculty of Medicine, Cairo University, in collaboration with the Microbiology and Immunology Department, Faculty of Pharmacy, and the Department of Medical Biochemistry and Molecular Biology, Faculty of Medicine, Fayoum University.

Disclosure statement

No potential conflict of interest was reported by the authors.