Calcitonin Improved Chondrocytes in Osteoarthritis through the Wnt Signaling Pathway

Osteoarthritis (OA) represents the most prevalent joint ailment among the elderly population. Calcitonin is an amino acid polypeptide produced and secreted by parathyroid C cells. Our research plans to reveal the underlying roles of calcitonin in OA pathogenesis.

Rat chondrocytes were treated with IL-1β to establish an OA model and randomly assigned to control, model, calcitonin, calcitonin+Ca2+, SKL2001, model+SKL2001, and model+SKL2001+calcitonin groups. ADAMTS4, COL2A1, COL1A1, and MMPs, cell proliferation, inflammatory cytokine levels, and reactive oxygen species (ROS) were measured to assess the effects of treatments and the involvement of the Wnt signaling pathway.

IL-1β-induced chondrocyte injury was successfully established. Calcitonin enhanced chondrocyte proliferation, upregulated COL2A1, and downregulated ADAMTS4 and MMP3, while reducing inflammatory cytokine production and ROS. Notably, co-treatment with Ca2+ partially reversed the protective effects of calcitonin. The presence of Ca2+ attenuated the suppression of WNT5A expression by calcitonin, suggesting that calcium can modulate its effect on Wnt signaling.

These findings indicate that calcitonin exerts chondroprotective effects in OA by promoting COL2A1 synthesis, suppressing catabolic enzymes, and reducing inflammation and oxidative stress through Wnt pathway modulation. Ca2+ can attenuate these effects, highlighting the importance of calcium homeostasis in calcitonin-mediated chondrocyte regulation.

Calcitonin demonstrates potential as a therapeutic strategy for OA, and its efficacy may be influenced by extracellular Ca2+ levels, providing mechanistic insights for optimizing calcitonin-based interventions.