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Neuroprotective effects of PrxI over-expression in an in vitro human Alzheimer's disease model

Authors

  • Annamaria Cimini,

    1. Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy
    2. Sbarro Institute for Cancer Research, Molecular Medicine, Center of Biotechnology College of Science, Technology Temple University Philadelphia, Pennsylvania 19122
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  • Roberta Gentile,

    1. Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy
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  • Francesco Angelucci,

    1. Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy
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  • Elisabetta Benedetti,

    1. Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy
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  • Giuseppina Pitari,

    1. Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy
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  • Antonio Giordano,

    Corresponding author
    1. Sbarro Institute for Cancer Research, Molecular Medicine, Center of Biotechnology College of Science, Technology Temple University Philadelphia, Pennsylvania 19122
    2. Department of Human Pathology and Oncology, University of Siena, Siena, Italy
    • Department of Human Pathology and Oncology, University of Siena, Strada delle Scotte n. 6, 53100 Siena, Italy.
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  • Rodolfo Ippoliti

    Corresponding author
    1. Department of Life, Health and Environmental Sciences, University of L'Aquila, L'Aquila, Italy
    • Department of Health, Life and Environmental Sciences, University of L'Aquila, via Vetoio n 10, 67100 L'Aquila, Italy.
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Abstract

Peroxiredoxins are ubiquitous proteins that recently attracted major interests in view of the strict correlation observed in several cell lines and/or tissues between different levels of their expression and the increased capacity of cells to survive in different pathophysiological conditions. They are recently considered as the most important enzymes regulating the concentration of hydroperoxides inside the cells. Most of neurodisorders such as Parkinson, Huntington, Alzheimer's diseases, and ischemic injury are characterized by conditions of oxidative stress inside cells. In these pathophysiological conditions, a strict correlation between cell survival and Prx expression has been found. In CNS all the Prx isoforms are present though with different expression pattern depending on cell phenotype. Interestingly, neurons treated with amyloid beta peptide (Aβ), showed an overexpression of PrxI. In this study, the neuroprotective effect of PrxI after Aβ exposure and the underlying mechanisms by which PrxI expression counteracts cell death was investigated in a well established human AD in vitro model. Taking advantage on cells transfected by a construct where human PrxI is fused with a Green fluorescent protein (GFP) at the C-terminus, we report some events at the basis of cell survival after Aβ injury, suggesting possible new signal cascades dealing with the antiapoptotic effect of PrxI. The results obtained indicated a protective role for PrxI in counteracting Aβ injury by increasing cell viability, preserving neurites, and decreasing cell death. J. Cell. Biochem. 114: 708–715, 2013. © 2012 Wiley Periodicals, Inc.

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