• Login
    View Item 
    •   Home
    • Centers & Institutes
    • Institute of Molecular Medicine and Genetics
    • Institute of Molecular Medicine and Genetics: Faculty Research and Presentations
    • View Item
    •   Home
    • Centers & Institutes
    • Institute of Molecular Medicine and Genetics
    • Institute of Molecular Medicine and Genetics: Faculty Research and Presentations
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of Scholarly CommonsCommunitiesTitleAuthorsIssue DateSubmit DateSubjectsThis CollectionTitleAuthorsIssue DateSubmit DateSubjects

    My Account

    LoginRegister

    About

    AboutCreative CommonsAugusta University LibrariesUSG Copyright Policy

    Statistics

    Display statistics

    Mitochondrial BNIP3 upregulation precedes endonuclease G translocation in hippocampal neuronal death following oxygen-glucose deprivation.

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    1471-2202-10-113.pdf
    Size:
    1.402Mb
    Format:
    PDF
    Download
    Authors
    Zhao, Shen-Ting
    Chen, Ming
    Li, Shu-Ji
    Zhang, Ming-Hai
    Li, Bo-Xing
    Das, Manas
    Bean, Jonathan C
    Kong, Ji-Ming
    Zhu, Xin-Hong
    Gao, Tian-Ming
    Issue Date
    2009-09-23
    URI
    http://hdl.handle.net/10675.2/48
    
    Metadata
    Show full item record
    Abstract
    BACKGROUND: Caspase-independent apoptotic pathways are suggested as a mechanism for the delayed neuronal death following ischemic insult. However, the underlying signalling mechanisms are largely unknown. Recent studies imply the involvement of several mitochondrial proteins, including endonuclease G (EndoG) and Bcl-2/adenovirus E1B 19 kDa-interacting protein (BNIP3), in the pathway of non-neuronal cells. RESULTS: In this report, using western blot analysis and immunocytochemistry, we found that EndoG upregulates and translocates from mitochondria to nucleus in a time-dependent manner in cultured hippocampal neurons following oxygen-glucose deprivation (OGD). Moreover, the translocation of EndoG occurs hours before the observable nuclear pyknosis. Importantly, the mitochondrial upregulation of BNIP3 precedes the translocation of EndoG. Forced expression of BNIP3 increases the nuclear translocation of EndoG and neuronal death while knockdown of BNIP3 decreases the OGD-induced nuclear translocation of EndoG and neuronal death. CONCLUSION: These results suggest that BNIP3 and EndoG play important roles in hippocampal neuronal apoptosis following ischemia, and mitochondrial BNIP3 is a signal protein upstream of EndoG that can induce neuronal death.
    Citation
    BMC Neurosci. 2009 Sep 8; 10:113
    ae974a485f413a2113503eed53cd6c53
    10.1186/1471-2202-10-113
    Scopus Count
    Collections
    Institute of Molecular Medicine and Genetics: Faculty Research and Presentations

    entitlement

    Related articles

    • BNIP3 upregulation and EndoG translocation in delayed neuronal death in stroke and in hypoxia.
    • Authors: Zhang Z, Yang X, Zhang S, Ma X, Kong J
    • Issue date: 2007 May
    • Reactive oxygen species-induced cell death of rat primary astrocytes through mitochondria-mediated mechanism.
    • Authors: Wang CC, Fang KM, Yang CS, Tzeng SF
    • Issue date: 2009 Aug 1
    • The proapoptotic member of the Bcl-2 family Bcl-2 / E1B-19K-interacting protein 3 is a mediator of caspase-independent neuronal death in excitotoxicity.
    • Authors: Zhang Z, Shi R, Weng J, Xu X, Li XM, Gao TM, Kong J
    • Issue date: 2011 Jan
    • The proapoptotic protein BNIP3 interacts with VDAC to induce mitochondrial release of endonuclease G.
    • Authors: Zhang X, Bian X, Kong J
    • Issue date: 2014
    • Arsenic trioxide induces autophagic cell death in malignant glioma cells by upregulation of mitochondrial cell death protein BNIP3.
    • Authors: Kanzawa T, Zhang L, Xiao L, Germano IM, Kondo Y, Kondo S
    • Issue date: 2005 Feb 3
    DSpace software (copyright © 2002 - 2021)  DuraSpace
    Quick Guide | Contact Us
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.