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Published on: January 31, 2020
miRNA-31 over-expression improve synovial cells apoptosis induced by RA
Objective:
The aim of this study was to evaluate the effects and mechanism of miRNA-31 in synovial cells apoptosis induced by RA.
Methods:
The miRNA-31 gene expressions were extracted from synovial tissues of normal and RA patients by RT-PCR and H et E staining. The synovial cells of RA patients were isolated and randomly divided into Control, Blank and miRNA groups. The cell apoptosis of difference groups were measured by flow cytometry; the TNF-α and IL-1β concentrations of difference groups were measured by Elisa assay; TLR4 and NF-κB proteins expressions were measured by WB assay and the correlation between TLR4 and miRNA-31 were evaluated by double luciferase target experiment.
Results:
The miRNA-31 gene expression was significantly suppressed in RA tissues (p<0.001); Compared with control group, the cell apoptosis rate of miRNA group was significantly suppressed (p<0.001); TNF-α and IL-1β concentrations were significantly down-regulation in culture fluid (p<0.001, respectively) and TLR4 and NF-κB proteins expressions were significantly depressed (p<0.001, respectively) in miRNA group. By double luciferase target experiment, the TLR4 was a target gene of miRNA-31.
Conclusion:
miRNA-31 is a key role in synovial cells apoptosis induced by RA (Fig. 7, Ref. 23).
Insights
MicroRNA-31 (miRNA-31) plays a crucial role in suppressing synovial cell apoptosis in rheumatoid arthritis (RA). Its downregulation in RA tissues contributes to increased inflammation and cell death, highlighting its therapeutic potential.
Area of Science:
- Molecular Biology
- Immunology
- Rheumatology
Background:
- Rheumatoid arthritis (RA) is characterized by synovial cell apoptosis.
- The role of microRNA-31 (miRNA-31) in RA pathogenesis is not fully understood.
Purpose of the Study:
- To investigate the effects and mechanism of miRNA-31 in synovial cell apoptosis induced by RA.
- To determine if miRNA-31 influences inflammatory markers and signaling pathways in RA.
Main Methods:
- Gene expression analysis of miRNA-31 in RA synovial tissues.
- Isolation and culture of synovial cells from RA patients.
- Assessment of cell apoptosis, inflammatory cytokine levels (TNF-α, IL-1β), and protein expression (TLR4, NF-κB).
- Luciferase reporter assays to validate miRNA-31 targeting of TLR4.
Main Results:
- miRNA-31 expression was significantly reduced in RA tissues.
- miRNA-31 suppressed synovial cell apoptosis, reduced TNF-α and IL-1β levels, and decreased TLR4 and NF-κB protein expression.
- TLR4 was identified as a direct target gene of miRNA-31.
Conclusions:
- miRNA-31 is a key regulator of synovial cell apoptosis in RA.
- Restoration of miRNA-31 levels may offer a therapeutic strategy for RA by reducing inflammation and apoptosis.
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