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Cox, Carly S.; McKay, Sharen E.; Holmbeck, Marissa A.; Christian, Brooke E.; Scortea, Andrew C.; Tsay, Annie J.; Newman, Laura E.; Shadel, Gerald S.
Cell metabolism, 11/2018, Letnik: 28, Številka: 5Journal Article
Transient mitochondrial stress can promote beneficial physiological responses and longevity, termed “mitohormesis.” To interrogate mitohormetic pathways in mammals, we generated mice in which mitochondrial superoxide dismutase 2 (SOD2) can be knocked down in an inducible and reversible manner (iSOD2-KD mice). Depleting SOD2 only during embryonic development did not cause post-natal lethality, allowing us to probe adaptive responses to mitochondrial oxidant stress in adult mice. Liver from adapted mice had increased mitochondrial biogenesis and antioxidant gene expression and fewer reactive oxygen species. Gene expression analysis implicated non-canonical activation of the Nrf2 antioxidant and PPARγ/PGC-1α mitochondrial signaling pathways in this response. Transient SOD2 knockdown in embryonic fibroblasts from iSOD2-KD mice also resulted in adaptive mitochondrial changes, enhanced antioxidant capacity, and resistance to a subsequent oxidant challenge. We propose that mitohormesis in response to mitochondrial oxidative stress in mice involves sustained activation of mitochondrial and antioxidant signaling pathways to establish a heightened basal antioxidant state. Display omitted •Inducible and reversible SOD2 knockdown mice (iSOD2-KD) have been developed•Embryonic mitochondrial oxidant stress results in adaptive changes in adult liver•Mitohormesis in adapted liver involves basal activation of PPARγ, PGC-1α, and Nrf2•Mitohormesis in iSOD2-KD embryonic fibroblasts provides resistance to oxidative stress A mouse model of inducible SOD2 gene knockdown reveals the existence of stable, adaptive responses in adult liver to mitochondrial oxidant stress during embryogenesis and in primary embryonic fibroblasts. These mitohormetic responses involve mitochondrial remodeling and priming of antioxidant pathways via basal activation of PPARγ, PGC-1α, and Nrf2 signaling.
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