Immune Netw.
2022 Apr;22(2):e14. 10.4110/in.2022.22.e14.
Mitochondrial Transplantation Ameliorates the Development and Progression of Osteoarthritis
- Affiliations
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- 1Rheumatism Research Center, College of Medicine, Catholic Research Institute of Medical Science, The Catholic University of Korea, Seoul 06591, Korea
- 2Department of Biomedicine & Health Sciences, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea
- 3Department of Orthopedic Surgery, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea
- 4Division of Rheumatology, Department of Internal Medicine, Seoul St. Mary's Hospital, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea
- 5Department of Medical Lifescience, College of Medicine, The Catholic University of Korea, Seoul 06591, Korea
- KMID: 2536241
- DOI: http://doi.org/10.4110/in.2022.22.e14
Abstract
- Osteoarthritis (OA) is a common degenerative joint disease characterized by breakdown of joint cartilage. Mitochondrial dysfunction of the chondrocyte is a risk factor for OA progression. We examined the therapeutic potential of mitochondrial transplantation for OA. Mitochondria were injected into the knee joint of monosodium iodoacetateinduced OA rats. Chondrocytes from OA rats or patients with OA were cultured to examine mitochondrial function in cellular pathophysiology. Pain, cartilage destruction, and bone loss were improved in mitochondrial transplanted-OA rats. The transcript levels of IL-1β, TNF-α, matrix metallopeptidase 13, and MCP-1 in cartilage were markedly decreased by mitochondrial transplantation. Mitochondrial function, as indicated by membrane potential and oxygen consumption rate, in chondrocytes from OA rats was improved by mitochondrial transplantation. Likewise, the mitochondrial function of chondrocytes from OA patients was improved by coculture with mitochondria. Furthermore, inflammatory cell death was significantly decreased by coculture with mitochondria. Mitochondrial transplantation ameliorated OA progression, which is caused by mitochondrial dysfunction. These results suggest the therapeutic potential of mitochondrial transplantation for OA.
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