Myasthenie.com

J Int Med Res. 2022 Jun;50(6):3000605211053703. doi: 10.1177/03000605211053703.

ABSTRACT

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.

PMID:35707849 | DOI:10.1177/03000605211053703


Source: https://pubmed.ncbi.nlm.nih.gov/3570784 ... 9&v=2.17.6