Melatonin differentially modulates chondro-osteogenic lineage commitment and suppresses proinflammatory mediator production in equine mesenchymal stem cells.

Melatonin preserves chondrogenic phenotype and suppresses inflammation in equine MSCs, supporting its therapeutic potential.

This in vitro experimental study investigated the effects of melatonin on equine mesenchymal stem cells (eMSCs) across three conditions: chondrogenic differentiation, osteogenic differentiation, and chondro-osteogenic transdifferentiation, with additional evaluation of its anti-inflammatory properties. Conducted between October 2023 and June 2024, the study measured gene expression of key chondrogenic (COLII, SOX9) and osteogenic (RUNX2, ALP, COLI) markers via quantitative RT-PCR, and quantified proinflammatory cytokines (IL-1β, TNF-α, IL-6, IL-8) in culture supernatants using multiplex immunoassay. Results demonstrated context-dependent effects of melatonin on lineage commitment. In chondrogenic cultures, melatonin enhanced COLII and SOX9 expression while maintaining favorable COLII:COLI and SOX9:RUNX2 ratios, supporting chondrogenic phenotype preservation. During chondro-osteogenic transdifferentiation, melatonin promoted an early osteogenic or hypertrophic shift by increasing RUNX2 and ALP while decreasing chondrogenic ratios. Conversely, in osteogenic cultures, melatonin suppressed RUNX2, ALP, and COLI expression, demonstrating inhibitory effects on osteogenic differentiation. Notably, melatonin consistently and significantly reduced all four proinflammatory cytokines across all culture conditions, suggesting a robust anti-inflammatory capacity independent of differentiation context. These findings highlight melatonin as a biologically active modulator of MSC lineage behavior and inflammatory responses in horses, warranting further investigation as a potential therapeutic adjunct in equine cartilage repair strategies and inflammatory musculoskeletal conditions.

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