• Login / Register
    View Item 
    •   Home
    • Support Departments
    • Harvested data
    • View Item
    •   Home
    • Support Departments
    • Harvested data
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of ChesterRepCommunitiesTitleAuthorsPublication DateSubmit DateSubjectsPublisherJournalThis CollectionTitleAuthorsPublication DateSubmit DateSubjectsPublisherJournalProfilesView

    My Account

    LoginRegister

    About

    AboutUniversity of Chester

    Statistics

    Display statistics

    Regucalcin ameliorates doxorubicin-induced cytotoxicity in Cos-7 kidney cells and translocates from the nucleus to the mitochondria.

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    article.pdf
    Size:
    1.219Mb
    Format:
    PDF
    Download
    Authors
    Mohammed, Noor A
    Hakeem, Israa J
    Hodges, Nikolas
    Michelangeli, Francesco; orcid: 0000-0002-4878-046X
    Publication Date
    2022-01-01
    
    Metadata
    Show full item record
    Abstract
    Doxorubicin (DOX) is a potent anticancer drug, which can have unwanted side-effects such as cardiac and kidney toxicity. A detailed investigation was undertaken of the acute cytotoxic mechanisms of DOX on kidney cells, using Cos-7 cells as kidney cell model. Cos-7 cells were exposed to DOX for a period of 24 h over a range of concentrations, and the LC50 was determined to be 7 µM. Further investigations showed that cell death was mainly via apoptosis involving Ca2+ and caspase 9, in addition to autophagy. Regucalcin (RGN), a cytoprotective protein found mainly in liver and kidney tissues, was overexpressed in Cos-7 cells and shown to protect against DOX-induced cell death. Subcellular localization studies in Cos-7 cells showed RGN to be strongly correlated with the nucleus. However, upon treatment with DOX for 4 h, which induced membrane blebbing in some cells, the localization appeared to be correlated more with the mitochondria in these cells. It is yet to be determined whether this translocation is part of the cytoprotective mechanism or a consequence of chemically induced cell stress.
    Citation
    Bioscience reports, volume 42, issue 1
    URI
    http://hdl.handle.net/10034/626659
    Type
    article
    Description
    From Europe PMC via Jisc Publications Router
    History: ppub 2022-01-01
    Publication status: Published
    Collections
    Harvested data

    entitlement

     
    DSpace software (copyright © 2002 - 2022)  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.