Mitochondria Transplant Therapy for Injured Skeletal Muscle
Uptake of donor mitochondria in myoblasts, myotubes and myofibres.
News Release, World Mitochondria Society, Berlin - Germany – January 12, 2023
- BaCl2 was injected into the gastrocnemius muscle of one limb of 8–12-week-old C57BL/6 mice to induce damage without injury to the resident stem cells.
- The contralateral gastrocnemius muscle was injected with phosphate-buffered saline (PBS) and served as the non-injured intra-animal control.
- Mitochondria were isolated from donor mice.
- Donor mitochondria were suspended in PBS or PBS without mitochondria (sham treatment) and injected into the tail vein of BaCl2 injured mice 24 h after the initial injury.
- Muscle repair was examined 7, 14 and 21 days after injury.
MTT did not increase systemic inflammation in mice. Muscle mass 7 days following injury was 21.9 ± 2.1% and 17.4 ± 1.9% lower (P < 0.05) in injured as compared with non-injured intra-animal control muscles in phosphate-buffered saline (PBS)- and MTT-treated animals, respectively.
Maximal plantar flexor muscle force was significantly lower in injured as compared with uninjured muscles of PBS-treated and MTT-treated mice, but the reduction in force was not different between the experimental groups. The percentage of collagen and other non-contractile tissue in histological muscle cross sections, was significantly greater in injured muscles of PBS-treated mice compared with MTT-treated mice 7 days after injury.
Muscle wet weight and maximal muscle force from injured MTT-treated mice had recovered to control levels by 14 days after the injury. However, muscle mass and force had not improved in PBS-treated animals by 14 days after injury.
By 21 days following injury, PBS-treated mice had fully restored gastrocnemius muscle mass of the injured muscle to that of the uninjured muscle, although maximal plantar flexion force was still lower in injured/repaired gastrocnemius as compared with uninjured intra-animal control muscles.
© Image - Alway et al., Journal of Cachexia, Sarcopenia and Muscle (2023)
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