AI Article Synopsis
- Synovial samples from 30 rheumatoid arthritis (RA) patients and 30 controls were used to isolate fibroblast-like synoviocytes (FLSs), revealing increased circ_0007707 expression in RA patients.
- Silencing circ_0007707 led to reduced cell proliferation, increased apoptosis, and lower inflammatory responses in FLS-RA cells, suggesting its role in disease progression.
- The mechanism involves circ_0007707 sponging miR-27b-3p, which in turn regulates PDE3B expression, highlighting circ_0007707 as a potential therapeutic target for RA.
Article Abstract
Synovial samples collected from 30 rheumatoid arthritis (RA) patients and 30 normal controls were used to isolate fibroblast-like synoviocytes (FLSs) and named FLS-RA and FLS-Normal, respectively. Real-time quantitative polymerase chain reaction (RT-qPCR) was utilized to detect circ_0007707 expression. Effects of circ_0007707 silencing on cell proliferation and apoptosis were evaluated using cell counting kit-8, 5-ethynyl-2'-deoxyuridine (Edu), and flow cytometry assays. Levels of pro-inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). Increased circ_0007707 expression was observed in synovial samples from RA patients and FLS-RA cells. Functional analysis showed circ_0007707 silencing restrained cell proliferation, induced cell apoptosis, and decreased cell inflammatory response in FLS-RA cells. Mechanistic analysis revealed the sponge function of circ_0007707 on miR-27b-3p, and miR-27b-3p inhibition weakened circ_0007707 knockdown-mediated effects on FLS-RA cell proliferation, apoptosis, and inflammatory response. Circ_0007707 could mediate PDE3B expression via sponging miR-27b-3p, and PDE3B overturned miR-27b-3p mimic-mediated effects on FLS-RA cell proliferation, apoptosis, and inflammatory response. Circ_0007707 mediated cell apoptosis and inflammatory response in FLS-RA cells through the miR-27b-3p/PDE3B axis, indicating the potential function of circ_0007707 as a target for RA treatment.
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| http://dx.doi.org/10.1016/j.intimp.2023.110157 | DOI Listing |
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