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      Experimental study on the neurotoxic effect of β-amyloid on the cytoskeleton of PC12 cells

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          Abstract

          The aim of the present study was to establish a cell model of Alzheimer's disease (AD) and investigate the neurotoxic effects of β-amyloid (Aβ) on the cytoskeleton. PC12 cells were cultured and treated with Aβ 25-35, and cell survival was analyzed with the MTT assay. Cell apoptosis was visualized using 4′,6-diamidino-2-phenylindole staining and the terminal deoxynucleotidyl transferase dUTP nick-end labeling assay. Immunocytochemistry and phalloidin staining were used to label the cytoskeleton of PC12 cells. Aβ 25-35 was found to induce PC12 cell apoptosis in a dose-dependent manner (P<0.05). Moreover, Aβ 25-35 also caused dose-dependent disintegration of the cytoskeleton (P<0.05). Therefore, the PC12 cell cytoskeleton was found to be sensitive to Aβ 25-35 neurotoxicity. The disintegration of the cytoskeleton is likely an important pathological alteration in AD, and Aβ is a key molecule involved in AD pathogenesis.

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          The neuroprotective roles of BDNF in hypoxic ischemic brain injury.

          MENG MAO, Kai-yu Tong, Jing Xiong … (2012)
          Hypoxia-ischemia (H/I) brain injury results in various degrees of damage to the body, and the immature brain is particularly fragile to oxygen deprivation. Hypothermia and erythropoietin (EPO) have long been known to be neuroprotective in ischemic brain injury. Brain-derived neurotrophic factor (BDNF) has recently been recognized as a potent modulator capable of regulating a wide repertoire of neuronal functions. This review was based on studies concerning the involvement of BDNF in the protection of H/I brain injury following a search in PubMed between 1995 and December, 2011. We initially examined the background of BDNF, and then focused on its neuroprotective mechanisms against ischemic brain injury, including its involvement in promoting neural regeneration/cognition/memory rehabilitation, angiogenesis within ischemic penumbra and the inhibition of the inflammatory process, neurotoxicity, epilepsy and apoptosis. We also provided a literature overview of experimental studies, discussing the safety and the potential clinical application of BDNF as a neuroprotective agent in the ischemic brain injury.
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            A role for the actin cytoskeleton in cell death and aging in yeast

            Campbell Gourlay, Lindsay Carpp, Paul Timpson … (2004)
            Several determinants of aging, including metabolic capacity and genetic stability, are recognized in both yeast and humans. However, many aspects of the pathways leading to cell death remain to be elucidated. Here we report a role for the actin cytoskeleton both in cell death and in promoting longevity. We have analyzed yeast strains expressing mutants with either increased or decreased actin dynamics. We show that decreased actin dynamics causes depolarization of the mitochondrial membrane and an increase in reactive oxygen species (ROS) production, resulting in cell death. Important, however, is the demonstration that increasing actin dynamics, either by a specific actin allele or by deletion of a gene encoding the actin-bundling protein Scp1p, can increase lifespan by over 65%. Increased longevity appears to be due to these cells producing lower than wild-type levels of ROS. Homology between Scp1p and mammalian SM22/transgelin, which itself has been isolated in senescence screens, suggests a conserved mechanism linking aging to actin stability.
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              Apoptosis is induced by beta-amyloid in cultured central nervous system neurons.

              C Cotman, Scott R Whittemore, A Copani … (1993)
              The molecular mechanism responsible for the neurodegeneration in Alzheimer disease is not known; however, accumulating evidence suggests that beta-amyloid peptide (A beta P) contributes to this degeneration. We now report that synthetic A beta Ps trigger the degeneration of cultured neurons through activation of an apoptotic pathway. Neurons treated with A beta Ps exhibit morphological and biochemical characteristics of apoptosis, including membrane blebbing, compaction of nuclear chromatin, and internucleosomal DNA fragmentation. Aurintricarboxylic acid, an inhibitor of nucleases, prevents DNA fragmentation and delays cell death. Our in vitro results suggest that apoptosis may play a role in the neuronal loss associated with Alzheimer disease.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Int J Mol Med
                Journal ID (iso-abbrev): Int. J. Mol. Med
                Journal ID (publisher-id): IJMM
                Title: International Journal of Molecular Medicine
                Publisher: D.A. Spandidos
                ISSN (Print): 1107-3756
                ISSN (Electronic): 1791-244X
                Publication date (Print): May 2018
                Publication date (Electronic): 07 February 2018
                Publication date PMC-release: 07 February 2018
                Volume: 41
                Issue: 5
                Pages: 2764-2770
                Affiliations
                [1 ]Institute of Neurobiology, College of Life Sciences, Henan University
                [2 ]College of Nursing, Henan University, Kaifeng, Henan 475004, P.R. China
                Author notes
                Correspondence to: Dr Jinbo Deng, Institute of Neurobiology, College of Life Sciences, Henan University, 1 Jinming Road, Kaifeng, Henan 475004, P.R. China, Email: jinbo_deng@ 123456henu.edu.cn
                Dr Jiexin Deng, College of Nursing, Henan University, 1 Jinming Road, Kaifeng, Henan 475004, P.R. China, E-mail: dengjiexin@ 123456yahoo.com
                [*]

                Contributed equally

                Article
                Publisher ID: ijmm-41-05-2764
                DOI: 10.3892/ijmm.2018.3467
                PMC ID: 5846656
                PubMed ID: 29436599
                SO-VID: b3b7b8a3-f46d-4e23-b31e-69b5a4b9cb49
                Copyright © Copyright: © Wang et al.
                License:

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

                History
                Date received : 05 July 2016
                Date accepted : 31 January 2018
                Categories
                Subject: Articles

                Keywords: alzheimer's disease,β-amyloid,cytoskeleton,neuroapoptosis,pc12 cells
                Data availability:
                Keywords: alzheimer's disease, β-amyloid, cytoskeleton, neuroapoptosis, pc12 cells

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