Long non-coding RNA growth arrest specific 5 regulates the T helper 17/regulatory T balance by targeting miR-23a in myasthenia gravis
| Autor: | Yingying Xu, Yiqun Ouyang |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2022 |
| Předmět: | |
| Zdroj: | Journal of International Medical Research, Vol 50 (2022) |
| Druh dokumentu: | article |
| ISSN: | 1473-2300 03000605 |
| DOI: | 10.1177/03000605211053703 |
| Popis: | Objective Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disorder. Recent studies report that long non-coding RNAs (lncRNAs) play vital roles in the pathogenesis of various diseases. This study explored the molecular mechanism of lncRNA growth arrest specific 5 (GAS5) in regulating the T helper 17 (Th17)/regulatory T (Treg) cell balance in MG. Methods GAS5 and miR-23a expression levels were detected by quantitative reverse transcription polymerase chain reaction. Flow cytometry was performed to examine the proportion of Th17 and Treg cells in CD4 + T cells from MG patients. The interaction between GAS5 and miR-23a was verified by luciferase reporter and RNA immunoprecipitation assays. Levels of Th17 and Treg-related proteins were examined using western blots and enzyme-linked immunosorbent assays. Results GAS5 expression levels were significantly decreased in the CD4 + T cells of MG patients, and GAS5 overexpression restrained Th17 differentiation in CD4 + T cells. Moreover, miR-23a was confirmed as a downstream target of GAS5 and negatively regulated by GAS5 through a direct interaction. Further exploration showed that GAS5 can inhibit Th17 differentiation by downregulating miR-23a. Conclusion Collectively, our results indicate that GAS5 can regulate the Th17/Treg balance by targeting miR-23a expression, providing a scientific basis for clinical therapeutic development for MG. |
| Databáze: | Directory of Open Access Journals |
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