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    Alpha-Endosulfine (ARPP-19e) expression in a rat model of stroke

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    Author
    Mehta, R.I.
    Tsymbalyuk, N.
    Ivanova, S.
    Date
    2017
    Journal
    Journal of Neuropathology and Experimental Neurology
    Publisher
    Oxford University Press
    Type
    Article
    
    Metadata
    Show full item record
    Other Titles
    α-Endosulfine (ARPP-19e) Expression in a Rat Model of Stroke
    See at
    https://www.doi.org/10.1093/jnen/nlx074
    Abstract
    In nutrient restricted environments, the yeast endosulfines Igo1/2 are activated via TORC1 inhibition and function critically to initiate and coordinate the cellular stress response that promotes survival. We examined expression of αEnsa, the mammalian homolog of yeast endosulfines, in rat stroke. Prominent neuronal upregulation of αEnsa was identified in 3 patterns within the ischemic gradient: (1) neurons in GFAP−/HSF1+ cortex showed upregulation and near-complete nuclear translocation of αEnsa protein within hours of ischemic onset; (2) neurons in GFAP+/HSF1+ cortex showed upregulation in cytoplasm and nuclei that persisted for days; (3) neurons in GFAP+/HSF1− cortex showed delayed cytosolic-only upregulation that persisted for days. Findings were corroborated using in situ hybridization for ENSA mRNA. Rapamycin treatment was found to reduce infarct size and behavioral deficits and, in GFAP+/HSF1+ zones, enhance αEnsa neuronal nuclear translocation and mitigate cell death, relative to controls. Based on the conservation of TOR signaling across species, and on the finding that the Rim15-Igo1/2-PP2A module is triggered by substrate deprivation in eukaryotic yeast, we speculate that αEnsa is activated by substrate deprivation, functioning through the homologous MASTL-αEnsa/ARPP19-PP2A module to promote neuronal survival. In conjunction with recent studies suggesting a neuroprotective role, our data highlight a potential function for αEnsa within ischemic brain. Copyright 2017 American Association of Neuropathologists, Inc.
    Sponsors
    This work was supported by grants to RIM from the Na-tional Institute of Neurological Disorders and Stroke (K08NS089830) and to JMS from the National Heart, Lung and Blood Institute (HL082517) and the National Institute of Neurological Disorders and Stroke (NS061808).
    Keyword
    Alpha-endosulfine
    Cerebral ischemia
    ENSA
    Molecular penumbra
    Nutrient deprivation
    Stroke
    Sulfonylurea receptor 1 (SUR1)
    αEnsa
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85030619919&doi=10.1093%2fjnen%2fnlx074&partnerID=40&md5=6fa7374264b4aa26d8411939d40c9025; http://hdl.handle.net/10713/9967
    ae974a485f413a2113503eed53cd6c53
    10.1093/jnen/nlx074
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