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Exogenous Hsc70, but not thermal preconditioning, confers protection to motoneurons subjected to oxidative stress.

Exogenous Hsc70, but not thermal preconditioning, confers protection to motoneurons subjected to oxidative stress. Research Abstract Details 

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  • Exogenous Hsc70, but not thermal preconditioning, confers protection to motoneurons subjected to oxidative stress. Abstract Text:

    mac b robinsonMac B Robinson,anna r taylorAnna R Taylor,david j gifondorwaDavid J Gifondorwa,michael tytellMichael Tytell,carolanne e milliganCarolanne E Milligan,mac b robinsonMac B Robinson,anna r taylorAnna R Taylor,david j gifondorwaDavid J Gifondorwa,michael tytellMichael Tytell,carolanne e milliganCarolanne E Milligan,mac b robinsonMac B Robinson,anna r taylorAnna R Taylor,david j gifondorwaDavid J Gifondorwa,michael tytellMichael Tytell,carolanne e milliganCarolanne E Milligan,

    Proper sensing of stress and the initiation of the stress response are critical to maintaining cell viability in response to noxious stimuli. Induction of the stress response prior to the exposure of a lethal stress (preconditioning) can be protective. Heat shock proteins (Hsps), the main products of the stress response, are considered to be responsible for this protective effect. Most cells readily initiate a stress response, but some neuronal phenotypes, including motoneurons (MNs), have a diminished capacity to do so. We have found that, given a proper stimulus, MNs can execute a heat stress response; but, it does not protect them from death caused by hydrogen peroxide (H(2)O(2)) induced oxidative stress, despite inhibiting H(2)O(2)-induced caspase activation. Conversely, we demonstrate that incubation with the heat shock cognate 70 (Hsc70) protein prior to oxidative insult can protect MNs from oxidative stress. This survival promoting effect may be mediated through the substrate binding domain (SBD) of Hsc70. Our data suggest that stress preconditioning may not be beneficial to MNs, but that pharmacological interventions and alternative means of acquiring components of the stress response are an effective means of ameliorating lethal stress in MNs and may be potentially useful therapeutically in preventing pathological MN loss. (c) 2007 Wiley Periodicals, Inc. Develop Neurobiol, 2008.

    Exogenous Hsc70, but not thermal preconditioning, confers protection to motoneurons subjected to oxidative stress. Publishing Authors By Initials

    mb robinsonMB Robinson,ar taylorAR Taylor,dj gifondorwaDJ Gifondorwa,m tytellM Tytell,ce milliganCE Milligan,mb robinsonMB Robinson,ar taylorAR Taylor,dj gifondorwaDJ Gifondorwa,m tytellM Tytell,ce milliganCE Milligan,mb robinsonMB Robinson,ar taylorAR Taylor,dj gifondorwaDJ Gifondorwa,m tytellM Tytell,ce milliganCE Milligan,

    For similar abstracts research abstracts see: abstracts research

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    Exogenous Hsc70, but not thermal preconditioning, confers protection to motoneurons subjected to oxidative stress. Journal Published:

    PUBLICATION TYPE: Journal Article

    Journal: Developmental neurobiology

    VOLUME: 68

    Page Numbers: 1-17

    Journal Abbreviation: Dev Neurobiol

    ISSN: 1932-8451

    DAY: 19

    MONTH: Jan

    YEAR: 2008

    Exogenous Hsc70, but not thermal preconditioning, confers protection to motoneurons subjected to oxidative stress. Information

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    LANGUAGE: eng

    NlmUniqueID: 101300215

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    Grant and Affiliation Information for Exogenous Hsc70, but not thermal preconditioning, confers protection to motoneurons subjected to oxidative stress.

    AFFILIATION: Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Winston-Salem, North Carolina 27157.

    Country: United States

    United States Research PublicationUnited States Research Publication

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    MEDLINETA: Dev Neurobiol

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