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  • Functional electron transport chain is necessary for stress resistance in quiescent cells

    Author(s)
    Novais, Silvia Magalhaes
    Blecha, Jan
    Rohlenova, Katerina
    Neuzil, Jiri
    Rohlena, Jakub
    Griffith University Author(s)
    Neuzil, Jiri
    Year published
    2018
    Metadata
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    Abstract
    Mitochondria are organelles central to energy metabolism and cell death. In the present work we investigated the role of functional electron transfer chain (ETC) in cell's adaptation to the quiescent state, using ETC-deficient (ρ0 cells) endothelial cell line EA.hy926 as a model. Preliminary results showed an increase in glucose consumption and lactate production in ETC-deficient quiescent cells compared to their proliferative counterparts. Unlike control cells, quiescent cells lacking the ETC were highly susceptible to reactive oxygen species (ROS) inducers such as phenethyl isothicyanate (PEITC). This was surprising, as ...
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    Mitochondria are organelles central to energy metabolism and cell death. In the present work we investigated the role of functional electron transfer chain (ETC) in cell's adaptation to the quiescent state, using ETC-deficient (ρ0 cells) endothelial cell line EA.hy926 as a model. Preliminary results showed an increase in glucose consumption and lactate production in ETC-deficient quiescent cells compared to their proliferative counterparts. Unlike control cells, quiescent cells lacking the ETC were highly susceptible to reactive oxygen species (ROS) inducers such as phenethyl isothicyanate (PEITC). This was surprising, as the ETC-deficient quiescent cells, similar to ETC-functional counterparts, showed elevated activity of mitochondrial antioxidant defense. Interestingly, we observed a reduced autophagic flux in quiescent ρ0 cells. Moreover, pharmacological interference with autophagy or the knock down of ATG5, a protein essential for autophagy, not only reduced autophagic flux but also increased sensitivity to ROS and the ROS-induced cell death in quiescent cells with functional ETC, recapitulating the ETC-deficient phenotype. This suggest that quiescent ETC-deficient cells are metabolically stressed, leading to compromised autophagic flux and limited protection from ROS.
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    Conference Title
    Free Radical Biology and Medicine
    Volume
    120
    DOI
    https://doi.org/10.1016/j.freeradbiomed.2018.04.262
    Subject
    Medicinal and Biomolecular Chemistry
    Biochemistry and Cell Biology
    Medical Biochemistry and Metabolomics
    Science & Technology
    Life Sciences & Biomedicine
    Endocrinology & Metabolism
    Molecular Biology
    Publication URI
    http://hdl.handle.net/10072/402386
    Collection
    • Conference outputs

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