Journal
BIOLOGY OPEN
Volume 4, Issue 5, Pages 622-626Publisher
COMPANY OF BIOLOGISTS LTD
DOI: 10.1242/bio.201511478
Keywords
Mitochondria; Transplantation; Cardioprotection; Mitochondrial DNA; Endocytosis
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Funding
- National Institutes of Health, National Heart Lung and Blood Institutes, Public Health Service Grant [HL103642]
- Anesthesia Research Distinguished Trailblazer Award, Boston Children's Hospital
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Previously, we have demonstrated that the transplantation of viable, structurally intact, respiration competent mitochondria into the ischemic myocardium during early reperfusion significantly enhanced cardioprotection by decreasing myocellular damage and enhancing functional recovery. Our in vitro and in vivo studies established that autologous mitochondria are internalized into cardiomyocytes following transplantation; however, the mechanism(s) modulating internalization of these organelles were unknown. Here, we show that internalization of mitochondria occurs through actin-dependent endocytosis and rescues cell function by increasing ATP content and oxygen consumption rates. We also show that internalized mitochondria replace depleted mitochondrial (mt)DNA. These results describe the mechanism for internalization of mitochondria within host cells and provide a basis for novel therapeutic interventions allowing for the rescue and replacement of damaged or impaired mitochondria.
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