Pyrroloquinoline quinone (PQQ), a redox-active o-quinone found in
various foods and mammalian tissues, has received an increasing amount
of attention because of a number of health benefits that can be
attributed to its ability to enhance mitochondrial biogenesis. However,
its underlying molecular mechanism remains incompletely understood. We
have now established that the exposure of mouse NIH/3T3 fibroblasts to a
physiologically relevant concentration of PQQ significantly stimulates
mitochondrial biogenesis.
The exposure of NIH/3T3 cells to 10–100 nM PQQ for 48 h resulted in
increased levels of Mitotracker staining, mitochondrial DNA content, and
mitochondrially encoded cytochrome c oxidase subunit 1 (MTCO1) protein.
Moreover, we observed that PQQ treatment induces deacetylation of the
peroxisome proliferator-activated receptor-γ-coactivator 1α (PGC-1α) and
facilitates its nuclear translocation and target gene expression but
does not affect its protein levels, implying increased activity of the
NAD+-dependent protein deacetylase sirtuin 1 (SIRT1).
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Indeed, treatment with a SIRT1 selective inhibitor, EX-527, hampered the
ability of PQQ to stimulate PGC-1α-mediated mitochondrial biogenesis.
We also found that the PQQ treatment caused a concentration-dependent
increase in the cellular NAD+ levels, but not the total NAD+ and NADH
levels. Our results suggest that PQQ-inducible mitochondrial biogenesis
can be attributed to activation of the SIRT1/PGC-1α signaling pathway by
enhancing cellular NAD+ formation.
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