Akademik Veri Yönetim Sistemi
15. World Congress on Targeting Mitochondria, Berlin, Almanya, 29 - 31 Ekim 2024, ss.50
Introduction: Osteoarthritis (OA), a degenerative disease characterized by progressive cartilage damage, mostly affects elderly people. Elevation in mitochondrial ROS production might accelerate cartilage degeneration and facilitate the development of OA. The alteration of mitochondrial function was associated with the OA pathogenesis.
Material & Methods: Inflammatory environmental stress mediated OA chondrocyte (OAC) model was conducted using conditioned medium (CM) of activated M1 polarized macrophages obtained by induction the U937 cells. hSF-MSC-derived chondrocytes were cultured in CM to create OAC. Mitochondria were obtained from Wharton’s-Jelly and bone-marrow derived mesenchymal stem cells (mt-WJ-MSC and mt-BM-MSC, respectively) and transferred naked. After 48 hours, ROS, MDA, ATP levels and HMOX-1 gene expression
were analyzed.
Results: Following isolation of mitochondria, transfer to OAC was confirmed by TMRM-staining. The intracellular ROS-level, which was increased after CM treatment, was dropped in mt-WJ-MSC and mt-BM-MSC groups, subsequent to mitochondrial transfer. MDA-levels displayed similar alterations. Compared to Control, HMOX-1 expression increased 2.8-fold in OAC, decreased 1.1-fold in mt-WJ-MSC, and increased 1.3-fold in mt-BM-MSC. ATP-levels significantly elevated in mt-WJ-MSC, whereas no effect was observed in
mt-BM-MSC.
Conclusion: mt-WJ-MSC and mt-BM-MSC transfers exhibit different effects on the antioxidant defense mechanisms in OAC. Age-related variations in mitochondria might play an important role in mitochondria-based therapy.