Shared more. Cited more. Safe forever.
    • advanced search
    • submit works
    • about
    • help
    • contact us
    • login
    View Item 
    •   MOspace Home
    • University of Missouri-Columbia
    • Graduate School - MU Theses and Dissertations (MU)
    • Theses and Dissertations (MU)
    • Dissertations (MU)
    • 2015 Dissertations (MU)
    • 2015 MU dissertations - Freely available online
    • View Item
    •   MOspace Home
    • University of Missouri-Columbia
    • Graduate School - MU Theses and Dissertations (MU)
    • Theses and Dissertations (MU)
    • Dissertations (MU)
    • 2015 Dissertations (MU)
    • 2015 MU dissertations - Freely available online
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.
    advanced searchsubmit worksabouthelpcontact us

    Browse

    All of MOspaceCommunities & CollectionsDate IssuedAuthor/ContributorTitleIdentifierThesis DepartmentThesis AdvisorThesis SemesterThis CollectionDate IssuedAuthor/ContributorTitleIdentifierThesis DepartmentThesis AdvisorThesis Semester

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular AuthorsStatistics by Referrer

    The role of the age-dependent loss of [alpha](E)-catenin in increased acute kidney injury /

    Wang, Xinhui, 1989-
    View/Open
    [PDF] public.pdf (2.159Kb)
    [PDF] research.pdf (4.329Mb)
    [PDF] short.pdf (98.99Kb)
    Date
    2015
    Format
    Thesis
    Metadata
    [+] Show full item record
    Abstract
    The aging kidney undergoes structural and functional alterations which make it more susceptible to acute kidney injury (AKI). Previous studies in our laboratory have shown that the aging kidney has a marked loss of alpha(E)-catenin in proximal tubular epithelium. alpha-Catenin, a key regulator of actin cytoskeleton, interacts with a variety of actin-binding proteins. Fascin 2 is an actin bundling protein that interacts with adhesion molecules and F-actin. In this work, we hypothesized that loss of alpha(E)-catenin leads to disruption of actin cytoskeleton which increases cisplatin-induced injury in aged kidney. A stable shRNA knock-down of alpha(E)-catenin was generated in NRK-52E cells (C2 cells); NT3 cells are the non-targeted control. We demonstrated that age-dependent loss of alpah(E)-catenin in renal tubule epithelial cells facilitates the Fas-mediated apoptotic signaling pathway in response to cisplatin-induced AKI injury. In addition, a cisplatin-induced loss of fascin 2 was observed in aged kidney. Overexpression of Fscn2 abolished increased cisplatin-induced apoptosis, mitochondrial dysfunction and oxidative stress in C2 cells compared with NT3 cells. In conclusion, this dissertation projects novel insight into understanding the increased incidence of AKI in aged kidney and identified a novel role of fascin 2 in renal epithelial cells, which depends on the functional interaction with alpha(E)-catenin and F-actin. These findings may lay the groundwork for new therapeutic approaches to AKI in aged patients in the future.
    URI
    https://hdl.handle.net/10355/57785
    https://doi.org/10.32469/10355/57785
    Degree
    Ph. D.
    Thesis Department
    Pharmacology (MU)
    Rights
    OpenAccess
    This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.
    Collections
    • 2015 MU dissertations - Freely available online
    • Medical Pharmacology and Physiology electronic theses and dissertations (MU)

    Send Feedback
    hosted by University of Missouri Library Systems
     

     


    Send Feedback
    hosted by University of Missouri Library Systems