The Growth Arrest-Specific Transcript 5 (GAS5) and Nuclear Receptor Subfamily 3 Group C Member 1 (NR3C1): Novel Markers Involved in Multiple Sclerosis.

Abstract

Recent studies have revealed that long noncoding RNAs (lncRNAs) are connected with pathogenesis of neurodegenerative diseases. Additionally, glucocorticoids have fundamental regulatory roles on the immune system, and act as potent therapeutic compounds for autoimmune and inflammatory diseases. The long noncoding RNA growth arrest-specific 5 (<i>GAS5</i>) which accumulates inside the cells in response to cellular starvation/growth arrest, acts as a potent repressor of the glucocorticoid receptor (GR) through its glucocorticoid response element (GRE). The aim of the present study was to investigate the role of lncRNA <i>GAS5</i> and its downstream target Nuclear Receptor Subfamily 3 Group C Member 1(<i>NR3C1</i>) in the pathogenesis of multiple sclerosis (MS), and to define the role of <i>GAS5</i> in the regulation of <i>NR3C1</i> expression. Quantitative polymerase chain reaction was performed for investigating the expression of <i>GAS5</i> and <i>NR3C1</i> in MS patients and healthy subjects. We found that <i>GAS5</i> levels were up-regulated in the MS patients, blood compared with healthy subjects in correlation with <i>NR3C1</i> expression. Our findings suggest that <i>GAS5</i> may play on important role in the molecular etiology and treatment of MS.