Related Experiment Videos
MicroRNA-652-3p Drives Chondrocyte Dysfunction in Post-Traumatic Osteoarthritis by Targeting γ-Glutamyl Carboxylase
Qinghai Han1, Suyi Wei2, Hong Wang3
1Orthopedic Rehabilitation Center 1, Beijing Rehabilitation Hospital, Capital Medical University, Beijing, 100144 China.
Background:
Post-traumatic osteoarthritis (PTOA) is a degenerative joint disorder initiated by trauma, with chondrocyte dysfunction and extracellular matrix (ECM) degradation as key pathological features. MicroRNA-652-3p (miR-652-3p) has been linked to osteoarthritis progression, but its role in PTOA remains unclear.
Objective:
This study sought to examine the predictive significance of miR-652-3p in PTOA development and elucidate its mechanistic role via targeting γ-glutamyl carboxylase (GGCX).
Methods:
Circulating miR-652-3p concentrations were measured in 100 PTOA cases and 70 healthy individuals using qRT-PCR. Diagnostic performance was evaluated by ROC analysis. Functional assays and rescue experiments were performed in IL-1β-stimulated C-28/12 chondrocytes. Direct targeting of GGCX by miR-652-3p was demonstrated through luciferase reporter assay.
Results:
Elevated miR-652-3p expression was significantly associated with PTOA (P < 0.001), demonstrating high diagnostic performance (AUC = 0.891). Logistic analysis identified its independent prognostic value for poor PTOA outcomes (OR = 4.789, P = 0.006). MiR-652-3p overexpression suppressed chondrocyte proliferation/migration, promoted apoptosis, and disrupted ECM homeostasis. Experimental validation identified GGCX as a direct downstream target of miR-652-3p, where GGCX silencing abolished the beneficial effects of miR-652-3p suppression.
Conclusion:
Our findings demonstrated that miR-652-3p drives PTOA pathogenesis by suppressing GGCX, highlighting its clinical potential as a combined biomarker and therapeutic candidate.
Supplementary Information:
The online version contains supplementary material available at https://doi.org/10.1007/s43465-026-01833-y.