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    STING-Mediated Autophagy Is Protective against H2O2-Induced Cell Death

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    Author
    Abdullah, A; Mobilio, F; Crack, PJ; Taylor, JM
    Date
    2020-10-01
    Source Title
    International Journal of Molecular Sciences
    Publisher
    MDPI
    University of Melbourne Author/s
    Taylor, Juliet; Crack, Peter; Abdullah, Amar; Mobilio, Frank
    Affiliation
    Pharmacology and Therapeutics
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Abdullah, A., Mobilio, F., Crack, P. J. & Taylor, J. M. (2020). STING-Mediated Autophagy Is Protective against H2O2-Induced Cell Death. INTERNATIONAL JOURNAL OF MOLECULAR SCIENCES, 21 (19), https://doi.org/10.3390/ijms21197059.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/251642
    DOI
    10.3390/ijms21197059
    Open Access at PMC
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7582849
    Abstract
    Stimulator of interferon genes (STING)-mediated type-I interferon signaling is a well characterized instigator of the innate immune response following bacterial or viral infections in the periphery. Emerging evidence has recently linked STING to various neuropathological conditions, however, both protective and deleterious effects of the pathway have been reported. Elevated oxidative stress, such as neuroinflammation, is a feature of a number of neuropathologies, therefore, this study investigated the role of the STING pathway in cell death induced by elevated oxidative stress. Here, we report that the H2O2-induced activation of the STING pathway is protective against cell death in wildtype (WT) MEFSV40 cells as compared to STING-/- MEF SV40 cells. This protective effect of STING can be attributed, in part, to an increase in autophagy flux with an increased LC3II/I ratio identified in H2O2-treated WT cells as compared to STING-/- cells. STING-/- cells also exhibited impaired autophagic flux as indicated by p62, LC3-II and LAMP2 accumulation following H2O2 treatment, suggestive of an impairment at the autophagosome-lysosomal fusion step. This indicates a previously unrecognized role for STING in maintaining efficient autophagy flux and protecting against H2O2-induced cell death. This finding supports a multifaceted role for the STING pathway in the underlying cellular mechanisms contributing to the pathogenesis of neurological disorders.

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