Journal
ANTIOXIDANTS
Volume 10, Issue 5, Pages -Publisher
MDPI
DOI: 10.3390/antiox10050696
Keywords
inflammation; apoptosis; mitochondrial dynamics; mitochondrial transplantation; tenocyte; tendinopathy
Funding
- National Research Foundation of Korea (NRF) - Korean government (MSIP) [2020R1F1A1048532]
- Bio and Medical Technology Development Program of the National Research Foundation of Korea (NRF) - Ministry of Science and ICT [NRF-2018M3A9B5023052]
- National Research Foundation of Korea [2020R1F1A1048532] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The study investigated the therapeutic effects of mitochondrial transplantation in a tendinopathy model by restoring damaged tenocytes and modulating inflammatory responses. Results indicated that mitochondrial transplantation could reduce oxidative stress, restore mitochondrial membrane potential, and downregulate fission markers in damaged tendon cells. Furthermore, the treatment showed promising results in reducing inflammation and promoting collagen production in a rat model of tendinopathy.
Tendinopathy is a common musculoskeletal condition causing pain and dysfunction. Conventional treatment and surgical procedures for tendinopathy are insufficient; accordingly, recent research has focused on tendon-healing regenerative approaches. Tendon injuries usually occur in the hypoxic critical zone, characterized by increased oxidative stress and mitochondrial dysfunction; thus, exogenous intact mitochondria may be therapeutic. We aimed to assess whether mitochondrial transplantation could induce anti-inflammatory activity and modulate the metabolic state of a tendinopathy model. Exogenous mitochondria were successfully delivered into damaged tenocytes by centrifugation. Levels of Tenomodulin and Collagen I in damaged tenocytes were restored with reductions in nuclear factor-kappa B and matrix metalloproteinase 1. The dysregulation of oxidative stress and mitochondrial membrane potential was attenuated by mitochondrial transplantation. Activated mitochondrial fission markers, such as fission 1 and dynamin-related protein 1, were dose-dependently downregulated. Apoptosis signaling pathway proteins were restored to the pre-damage levels. Similar changes were observed in a collagenase injection-induced rat model of tendinopathy. Exogenous mitochondria incorporated into the Achilles tendon reduced inflammatory and fission marker levels. Notably, collagen production was restored. Our results demonstrate the therapeutic effects of direct mitochondrial transplantation in tendinopathy. These effects may be explained by alterations in anti-inflammatory and apoptotic processes via changes in mitochondrial dynamics.
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