Author/Authors :
Gharesouran, Jalal Department of Medical Genetics- Shahid Beheshti University of Medical Sciences, Tehran , Taheri, Mohammad Department of Medical Genetics- Shahid Beheshti University of Medical Sciences, Tehran , Sayad, Arezou Department of Medical Genetics- Shahid Beheshti University of Medical Sciences, Tehran , Ghafouri-Fard, Soudeh Department of Medical Genetics- Shahid Beheshti University of Medical Sciences, Tehran , Mazdeh, Mehrdokht Neurophysiology Research Center- Hamadan University of Medical Sciences, Hamadan , Omrani, Mir Davood Department of Medical Genetics- Shahid Beheshti University of Medical Sciences, Tehran
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 (GAS5) 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 GAS5 and its downstream target Nuclear Receptor Subfamily 3 Group C Member 1(NR3C1) in the pathogenesis of multiple sclerosis (MS), and to define the role of GAS5 in the regulation of NR3C1 expression. Quantitative polymerase chain reaction was performed for investigating the expression of GAS5 and NR3C1 in MS patients and healthy subjects. We found that GAS5 levels were up-regulated in the MS patients, blood compared with healthy subjects in correlation with NR3C1 expression. Our findings suggest that GAS5 may play on important role in the molecular etiology and treatment of MS.
