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자료유형
학술저널
저자정보
A Ram Lee (The Catholic University of Korea) Jin Seok Woo (The Catholic University of Korea) Seon-Yeong Lee (The Catholic University of Korea) Hyun Sik Na (The Catholic University of Korea) Keun-Hyung Cho (The Catholic University of Korea) Yeon Su Lee (The Catholic University of Korea) Jeong Su Lee (The Catholic University of Korea) Seon Ae Kim (The Catholic University of Korea) Sung-Hwan Park (The Catholic University of Korea) Seok Jung Kim (The Catholic University of Korea) Mi-La Cho (The Catholic University of Korea)
저널정보
대한면역학회 Immune Network Immune Network Vol.22 No.2
발행연도
2022.4
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1 - 17 (17page)

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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 iodoacetate-induced 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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ABSTRACT
INTRODUCTION
MATERIALS AND METHODS
RESULTS
DISCUSSION
REFERENCES

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