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  • 1
    Online Resource
    Online Resource
    Nitro-Oxidative Stress after Neuronal Ischemia Induces Protein Nitrotyrosination and Cell Death
    Hindawi Limited ; 2013
    In:  Oxidative Medicine and Cellular Longevity Vol. 2013 ( 2013), p. 1-9
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2013 ( 2013), p. 1-9
    Abstract: Ischemic stroke is an acute vascular event that obstructs blood supply to the brain, producing irreversible damage that affects neurons but also glial and brain vessel cells. Immediately after the stroke, the ischemic tissue produces nitric oxide (NO) to recover blood perfusion but also produces superoxide anion. These compounds interact, producing peroxynitrite, which irreversibly nitrates protein tyrosines. The present study measured NO production in a human neuroblastoma (SH-SY5Y), a murine glial (BV2), a human endothelial cell line (HUVEC), and in primary cultures of human cerebral myocytes (HC-VSMCs) after experimental ischemia in vitro . Neuronal, endothelial, and inducible NO synthase (NOS) expression was also studied up to 24 h after ischemia, showing a different time course depending on the NOS type and the cells studied. Finally, we carried out cell viability experiments on SH-SY5Y cells with H 2 O 2 , a prooxidant agent, and with a NO donor to mimic ischemic conditions. We found that both compounds were highly toxic when they interacted, producing peroxynitrite. We obtained similar results when all cells were challenged with peroxynitrite. Our data suggest that peroxynitrite induces cell death and is a very harmful agent in brain ischemia.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2013/826143
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2013
    detail.hit.zdb_id: 2455981-7
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  • 2
    Online Resource
    Online Resource
    Amyloid Beta-Peptide Increases BACE1 Translation through the Phosphorylation of the Eukaryotic Initiation Factor-2 α
    Hindawi Limited ; 2020
    In:  Oxidative Medicine and Cellular Longevity Vol. 2020 ( 2020-09-21), p. 1-12
    Details
    In: Oxidative Medicine and Cellular Longevity, Hindawi Limited, Vol. 2020 ( 2020-09-21), p. 1-12
    Abstract: Alzheimer’s disease (AD) is tightly linked to oxidative stress since amyloid beta-peptide (A β ) aggregates generate free radicals. Moreover, the aggregation of A β is increased by oxidative stress, and the neurotoxicity induced by the oligomers and fibrils is in part mediated by free radicals. Interestingly, it has been reported that oxidative stress can also induce BACE1 transcription and expression. BACE1 is the key enzyme in the cleavage of the amyloid precursor protein to produce A β , and the expression of this enzyme has been previously shown to be enhanced in the brains of Alzheimer’s patients. Here, we have found that BACE1 expression is increased in the hippocampi from AD patients at both the early (Braak stage II) and late (Braak stage VI) stages of the disease as studied by immunohistochemistry and western blot. To address the role of A β and oxidative stress in the regulation of BACE1 expression, we have analyzed the effect of subtoxic concentrations of A β oligomers (0.25  μ M) and H 2 O 2 (10 mM) on a human neuroblastoma cell line. Firstly, our results show that A β oligomers and H 2 O 2 induce an increase of BACE1 mRNA as we studied by qPCR. Regarding BACE1 translation, it is dependent on the phosphorylation of the eukaryotic initiation factor 2 α (eIF2 α ), since BACE1 mRNA bears a 5 ′ UTR that avoids its translation under basal conditions. BACE1 5 ′ UTR contains four upstream initiating codons (uAUGs), and its translation is activated when eIF2 α is phosphorylated. Consistently, we have obtained that A β oligomers and H 2 O 2 increase the levels of BACE1 and p-eIF2 α assayed by western blot and confocal microscopy. Our results suggest that A β oligomers increase BACE1 translation by phosphorylating eIF2 α in a process that involves oxidative stress and conforms a pathophysiological loop, where the A β once aggregated favors its own production continuously by the increase in BACE1 expression as observed in AD patients.
    Type of Medium: Online Resource
    ISSN: 1942-0900 , 1942-0994
    URL: Article
    DOI: 10.1155/2020/2739459
    Language: English
    Publisher: Hindawi Limited
    Publication Date: 2020
    detail.hit.zdb_id: 2455981-7
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
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