Rice Univesrity Logo
    • FAQ
    • Deposit your work
    • Login
    View Item 
    •   Rice Scholarship Home
    • Faculty & Staff Research
    • Faculty Publications
    • View Item
    •   Rice Scholarship Home
    • Faculty & Staff Research
    • Faculty Publications
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Differential Aortic and Mitral Valve Interstitial Cell Mineralization and the Induction of Mineralization by Lysophosphatidylcholine In Vitro

    Thumbnail
    Name:
    nihms633760.pdf
    Size:
    976.7Kb
    Format:
    PDF
    View/Open
    Author
    Wiltz, Dena C.; Han, Richard I.; Wilson, Reid L.; Kumar, Aditya; Morrisett, Joel D.; More... Grande-Allen, K. Jane Less...
    Date
    2014
    Abstract
    Calcific aortic valve disease (CAVD) is a serious condition with vast uncertainty regarding the precise mechanism leading to valve calcification. This study was undertaken to examine the role of the lipid lysophosphatidylcholine (LPC) in a comparison of aortic and mitral valve cellular mineralization. The proportion of LPC in differentially calcified regions of diseased aortic valves was determined using thin layer chromatography (TLC). Next, porcine valvular interstitial cells (pVICs) from the aortic (paVICs) and mitral valve (pmVICs) were cultured with LPC (10−1–105 nM) and analyzed for cellular mineralization, alkaline phosphatase activity (ALPa), proliferation, and apoptosis. TLC showed a higher percentage of LPC in calcified regions of tissue compared to non-calcified regions. In pVIC cultures, with the exception of 105 nM LPC, increasing concentrations of LPC led to an increase in phosphate mineralization. Increased levels of calcium content were exhibited at 104 nm LPC application compared to baseline controls. Compared to pmVIC cultures, paVIC cultures had greater total phosphate mineralization, ALPa, calcium content, and apoptosis, under both a baseline control and LPC-treated conditions. This study showed that LPC has the capacity to promote pVIC calcification. Also, paVICs have a greater propensity for mineralization than pmVICs. LPC may be a key factor in the transition of the aortic valve from a healthy to diseased state. In addition, there are intrinsic differences that exist between VICs from different valves that may play a key role in heart valve pathology.
    Citation
    Wiltz, Dena C., Han, Richard I., Wilson, Reid L., et al.. "Differential Aortic and Mitral Valve Interstitial Cell Mineralization and the Induction of Mineralization by Lysophosphatidylcholine In Vitro." Cardiovascular Engineering and Technology, 5, no. 4 (2014) Springer: 371-383. http://dx.doi.org/10.1007/s13239-014-0197-3.
    Published Version
    http://dx.doi.org/10.1007/s13239-014-0197-3
    Keyword
    aortic valve; calcification; lipid; mitral valve
    Type
    Journal article
    Publisher
    Springer
    Citable link to this page
    https://hdl.handle.net/1911/87882
    Rights
    This is an author's peer-reviewed final manuscript, as accepted by the publisher. The published article is copyrighted by Springer.
    Metadata
    Show full item record
    Collections
    • Bioengineering Publications [632]
    • Faculty Publications [4990]

    Home | FAQ | Contact Us | Privacy Notice | Accessibility Statement
    Managed by the Digital Scholarship Services at Fondren Library, Rice University
    Physical Address: 6100 Main Street, Houston, Texas 77005
    Mailing Address: MS-44, P.O.BOX 1892, Houston, Texas 77251-1892
    Site Map

     

    Searching scope

    Browse

    Entire ArchiveCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsTypeThis CollectionBy Issue DateAuthorsTitlesSubjectsType

    My Account

    Login

    Statistics

    View Usage Statistics

    Home | FAQ | Contact Us | Privacy Notice | Accessibility Statement
    Managed by the Digital Scholarship Services at Fondren Library, Rice University
    Physical Address: 6100 Main Street, Houston, Texas 77005
    Mailing Address: MS-44, P.O.BOX 1892, Houston, Texas 77251-1892
    Site Map