Long noncoding RNA CHRF exacerbates IL-6-induced inflammatory damages by downregulating microRNA-146a in ATDC5 cells

Area of Science:

• Biochemistry
• Molecular Biology
• Cell Biology

Background:

• Osteoarthritis (OA) is a prevalent musculoskeletal disorder with limited effective treatments.
• Interleukin-6 (IL-6) plays a significant role in OA pathogenesis and inflammation.
• Long noncoding RNAs (lncRNAs) are emerging as key regulators in various cellular processes, including inflammation.

Purpose of the Study:

• To investigate the role of lncRNA CHRF in IL-6-induced inflammatory damage in vitro.
• To elucidate the regulatory mechanism of lncRNA CHRF in osteoarthritis.
• To explore the downstream targets and signaling pathways affected by lncRNA CHRF.

Main Methods:

• ATDC5 cells were treated with IL-6.
• Cell viability assessed using CCK-8 assay.
• Apoptosis evaluated by flow cytometry and western blot.
• Inflammatory factors measured by RT-qPCR, ELISA, and western blot.
• Expression levels of lncRNA CHRF and miR-146a were analyzed.

Main Results:

• IL-6 treatment reduced cell viability, increased apoptosis, and elevated inflammatory factors.
• IL-6 upregulated lncRNA CHRF and downregulated miR-146a.
• Overexpression of lncRNA CHRF exacerbated IL-6 effects, while knockdown ameliorated them.
• lncRNA CHRF negatively regulated miR-146a, and miR-146a overexpression counteracted lncRNA CHRF's effects.
• lncRNA CHRF promoted IL-6-induced activation of NF-κB and JAK1/STAT3 signaling pathways.

Conclusions:

• lncRNA CHRF aggravates IL-6-induced inflammatory damage in ATDC5 cells.
• The mechanism involves lncRNA CHRF downregulating miR-146a, leading to NF-κB and JAK1/STAT3 pathway activation.
• lncRNA CHRF represents a potential therapeutic target for osteoarthritis.