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Beta-amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes

Abstract : Accumulation of beta-amyloid peptide (Abeta), which is a landmark of Alzheimer's disease, may alter astrocyte functions before any visible symptoms of the disease occur. Here, we examined the effects of Abeta on biosynthesis and release of diazepam-binding inhibitor (DBI), a polypeptide primarily expressed by astroglial cells in the CNS. Quantitative RT-PCR and specific radioimmunoassay demonstrated that aggregated Abeta(25-35), at concentrations up to 10(-4) m, induced a dose-dependent increase in DBI mRNA expression and DBI-related peptide release from cultured rat astrocytes. These effects were totally suppressed when aggregation of Abeta(25-35) was prevented by Congo red. Measurement of the number of living cells revealed that Abeta(25-35) induced a trophic rather than a toxic effect on astrocytes. Administration of cycloheximide blocked Abeta(25-35)-induced increase of DBI gene expression and endozepine accumulation in astrocytes, indicating that protein synthesis is required for DBI gene expression. Altogether, the present data suggest that Abeta-induced activation of endozepine biosynthesis and release may contribute to astrocyte proliferation associated with Alzheimer's disease.
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Contributor : Jérôme Leprince <>
Submitted on : Tuesday, January 8, 2019 - 4:39:15 PM
Last modification on : Monday, July 20, 2020 - 1:06:06 PM

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Tursonjan Tokay, Olfa Masmoudi, Pierrick Gandolfo, Jérôme Leprince, Georges Pelletier, et al.. Beta-amyloid peptides stimulate endozepine biosynthesis in cultured rat astrocytes. Journal of Neurochemistry, Wiley, 2005, 94 (3), pp.607-616. ⟨10.1111/j.1471-4159.2005.03102.x⟩. ⟨hal-01974260⟩



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