Back to Search
Start Over
LncRNA GAS5 activates the AMPK pathway in peripheral blood mononuclear cells derived from rheumatoid arthritis patients.
- Source :
-
International Journal of Rheumatic Diseases . Oct2020, Vol. 23 Issue 10, p1318-1327. 10p. - Publication Year :
- 2020
-
Abstract
- Background: Rheumatoid arthritis (RA) is an inflammatory disease, which seriously affects human joints. This study aimed to detect the changes in the expression of long non‐coding RNA growth arrest‐specific transcript 5 (GAS5) in peripheral blood mononuclear cells (PBMCs) derived from patients with RA and healthy controls (HC), as well as analyze the correlation between GAS5 and clinical indicators of RA. Also, the role and mechanism of GAS5 in regulating the AMP‐activated protein kinase (AMPK) pathway in RA was further assessed. Methods: The PBMCs were isolated from the RA patients. Next, GAS5 expression was detected in RA PBMCs by quantitative real‐time polymerase chain reaction, and its diagnostic value on RA was determined by receiver operating characteristic curves (ROC). The levels of interleukin (IL)‐6 and IL‐17 were detected via enzyme‐linked immunosorbent assay. The expressions of total and phosphorylated AMPK as well as p38MAPK were determined with Western blot. Results: GAS5 was down‐regulated in RA PBMCs, and consequently serves as a potential diagnostic marker for RA (sensitivity, 90%; specificity, 80%; area under the curve, 0.89). Further, GAS5 negatively regulated erythrocyte sedimentation rate, C‐reactive protein, Disease Activity Score of 28 joints and antibodies against cyclic citrullinated peptide, as well as the IL‐6 and IL‐17 levels of RA PBMCs. Similarly, GAS5 was observed to activate the AMPK pathway. Conclusion: GAS5 activated the AMPK pathway, while it negatively regulated the expression of cytokines IL‐6 and IL‐17. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 17561841
- Volume :
- 23
- Issue :
- 10
- Database :
- Academic Search Index
- Journal :
- International Journal of Rheumatic Diseases
- Publication Type :
- Academic Journal
- Accession number :
- 146468797
- Full Text :
- https://doi.org/10.1111/1756-185X.13930