• Login
    View Item 
    •   UMB Digital Archive
    • School, Graduate
    • Theses and Dissertations All Schools
    • View Item
    •   UMB Digital Archive
    • School, Graduate
    • Theses and Dissertations All Schools
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of UMB Digital ArchiveCommunitiesPublication DateAuthorsTitlesSubjectsThis CollectionPublication DateAuthorsTitlesSubjects

    My Account

    LoginRegister

    Statistics

    Display statistics

    Regulation of calcium entry mechanisms by intracellular calcium pools

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Find Full text
    Author
    Ufret-Vincenty, Carmen Angeles
    Advisor
    Gill, Donald L.
    Date
    1998
    Type
    dissertation
    
    Metadata
    Show full item record
    Abstract
    Release of Ca2+ from intracellular pools is the main trigger for activation of Ca2+ entry during the generation of Ca2+ signals in non-excitable cells. The aim of these studies is to investigate the relationship between Ca2+ pool emptying and activation of Ca2+ influx. Using the smooth muscle cell line, DDT1MF-2, changes in cytosolic Ca2+ concentration were monitored by loading cells with the fluorescent Ca2+ indicator, fura-2. The studies reveal that Ca2+ pool depletion by treatment with the SERCA pump inhibitors, thapsigargin and 2,5-Di-tert-butylhydroquinone (DBHQ), stimulates the activation of a novel and distinct Ca2+ entry pathway sensitive to caffeine. Refilling of Ca2+ pools occurs concomitantly with the disappearance of the caffeine-sensitive Ca2+ entry pathway. Stimulation of the caffeine-sensitive Ca2+ entry pathway occurs independently of the means used to deplete intracellular Ca2+ pools (pump inhibition or ionophore-induced depletion). Therefore, activation of the caffeine-sensitive Ca2+ entry pathway is directly controlled by Ca2+ pool depletion. Ion permeability studies indicate that the Ca2+ entry pathway sensitive to caffeine is less selective for Ca2+ than store-operated Ca2+ entry, the major Ca2+ influx pathway activated by pool depletion in a wide variety of cells. Nitric oxide-induced thiol modification (nitrosylation) has recently been shown to have major modulatory effects on the activity of several Ca2+ channels. Therefore, it was important to investigate the role of thiol nitrosylation in controlling Ca2+ entry and its activation by pool depletion. Studies reveal that nitric oxide donors activate a substantial entry of Ca2+ through a direct pathway which is independent of guanylate cyclase activation, a well-studied target for nitric oxide. Cell permeant alkylating agents activate an entry of Ca2+ remarkably similar to nitric oxide-induced Ca2+ entry, indicating that activation of Ca2+ entry relies on modification of one or more thiol residues in the channel or a closely associated protein. Most significantly, Ca2+ pool emptying strongly stimulates the Ca2+ entry activated by both nitric oxide donors and alkylating agents, revealing a direct link between thiol nitrosylation and activation of a store-sensitive Ca2+ entry pathway. These studies provide further evidence for the strong involvement of Ca2+ pool content in controlling the activity of major Ca2+ entry mechanisms.
    Description
    University of Maryland, Baltimore. Biochemistry and Molecular Biology. Ph.D. 1998
    Keyword
    Biology, Cell
    calcium entry mechanisms
    calcium pools
    Calcium Signaling
    Identifier to cite or link to this item
    http://hdl.handle.net/10713/1361
    Collections
    Theses and Dissertations School of Medicine
    Theses and Dissertations All Schools

    entitlement

     
    DSpace software (copyright © 2002 - 2023)  DuraSpace
    Quick Guide | Policies | Contact Us | UMB Health Sciences & Human Services Library
    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.