The following is a summary of “MiR-98-5p plays suppressive effects on IL-1β-induced chondrocyte injury associated with osteoarthritis by targeting CASP3,” published in the April 2024 issue of Surgery by Lv et al.

Quantitative real-time PCR assessed miR-98-5p and CASP3 mRNA levels in OA cartilage tissues and IL-1β-treated CHON-001 cells. TargetScan was utilized for miR-98-5p and CASP3 binding site prediction, with confirmation via luciferase reporter assays. Chondrocyte viability was evaluated using CCK-8 assays, while pro-inflammatory cytokines (IL-1β, IL-6, TNF-α) were quantified via ELISA. Caspase-3 activity was measured to gauge apoptosis, and Western blotting was performed for protein marker quantification.

The findings revealed diminished miR-98-5p levels in both OA cartilage and IL-1β-stimulated cells. Augmented miR-98-5p expression correlated with reduced pro-inflammatory cytokines, decreased caspase-3 activity, and enhanced cell viability. Additionally, miR-98-5p overexpression hindered IL-1β-induced ECM degradation, evidenced by decreased MMP-13 and β-catenin levels, alongside increased COL2A1 expression. Notably, miR-98-5p’s modulation of CASP3 mRNA directly impacted its expression. Mimicking miR-98-5p’s effects, CASP3 knockdown inhibited IL-1β-induced inflammation, apoptosis, and ECM degradation. Conversely, CASP3 overexpression counteracted the suppressive effects of miR-98-5p.

In summary, the collective data underscore miR-98-5p’s protective role against IL-1β-induced chondrocyte damage through CASP3 targeting, suggesting its potential as a therapeutic target for OA.

Source: josr-online.biomedcentral.com/articles/10.1186/s13018-024-04628-9