Mitochondrial damage is commonly involved in liver injury. We have previously shown that normal mitochondria can be coated with a carrier protein to form complexes that are specifically taken up by liver cells in culture.
The aim of the current study was to determine whether mitochondrial complexes could be specifically delivered to the livers of living rats by intravenous injection.Mitochondria were harvested from fresh mouse liver, mixed with an asialoglycoprotein-based carrier, asialoorosomucoid-polylysine (AsOR-PL), and purified to form complexes.
To facilitate release of internalized mitochondria from endosomes, an endosomolytic peptide, listeriolysin O (LLO) was coupled to AsOR to form AsOR-LLO. Mitochondria alone, mitochondrial complexes with AsOR-PL, and mitochondrial complexes plus AsOR-LLO conjugate all containing the same number of mitochondria were injected intravenously.
Animals were sacrificed, and organs removed and analyzed by quantitative polymerase chain reaction (qPCR) of mouse mitochondrial DNA, electronmicroscopy (EM), and in situ PCR and hybridization followed by immunohistochemical analyses.Calculations revealed that approximately 27% of the total injected mitochondria was detected in liver, while less than 2% was found in spleen, and <1% in lungs.
 Recombinant Human FKBP6 Protein, His, -1mg |
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Immunohistochemistry showed that mouse mitochondrial DNA staining was minimal with mitochondrial complexes alone, strong periportal with mitochondrial complexes co-injected with AsOR-LLO, and absent with mitochondria alone.Targetable mitochondrial complexes can be delivered to rat liver, and the efficiency of that process is greatly enhanced by co-injection of a targetable endosomal release agent, AsOR-LLO.
