• Login
    View Item 
    •   SMARTech Home
    • Undergraduate Research Opportunities Program (UROP)
    • Undergraduate Research Option Theses
    • View Item
    •   SMARTech Home
    • Undergraduate Research Opportunities Program (UROP)
    • Undergraduate Research Option Theses
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Modulation of Cardiac Macrophages with Interleukin-4 as a Strategy of Infarct Healing

    Thumbnail
    View/Open
    CARROLL-UNDERGRADUATERESEARCHOPTIONTHESIS-2015.pdf (62.69Mb)
    Date
    2015-12
    Author
    Carroll, Sheridan
    Metadata
    Show full item record
    Abstract
    Cardiovascular disease is the leading cause of death in the United States accounting for approximately 1 in every 3 deaths. Many efforts have been made to reduce the mortality rate after a MI by analyzing and possibly manipulating the immune system response following an MI. Immediately after an MI has occurred, pro-inflammatory macrophages (M1) are recruited at the affected site. M1 are responsible for clearing dead cells and debris. Following the M1 response, wound healing (M2) macrophages, responsible for angiogenesis and cell regeneration, are recruited at the site. Although the M1 subset is required for proper wound healing, prolonged activation of this macrophage subset attributes to cell fibrosis and tissue scaring. This study initially aims in modulation of macrophages to a M2 phenotype utilizing IL-4 after an MI occurs. The secondary aim is delivery of IL-4 to the heart site utilizing a PEG-MAL hydrogel. This study could prove that delivery of IL-4 to the heart could suppress inflammatory signals after an MI and lead to a healing response. In vitro studies in RAW and bone marrow macrophages indicated IL-4 leads to an increase in the MRC1 and Arginase 1, M2 markers, and macrophages stimulated with lipopolysaccharide (LPS) and interferon gamma increased M1 markers nitrite and tumor necrosis factor alpha. The addition of both M1 and M2 stimuli simultaneously increased Arginase 1 and nitrite production significantly. The IL-4 treated media from the In vitro macrophages increased cardiac progenitor cell migration by 70% relative to the control. This shows that IL-4 differentiated macrophages can communicate with other cells crucial to healing. Knowledge of the effects of IL-4 after a heart attack could greatly improve cardiac cell regeneration and lead to better patient health.
    URI
    http://hdl.handle.net/1853/60321
    Collections
    • Department of Biomedical Engineering Undergraduate Research Option Theses [214]
    • Undergraduate Research Option Theses [862]

    Browse

    All of SMARTechCommunities & CollectionsDatesAuthorsTitlesSubjectsTypesThis CollectionDatesAuthorsTitlesSubjectsTypes

    My SMARTech

    Login

    Statistics

    View Usage StatisticsView Google Analytics Statistics
    facebook instagram twitter youtube
    • My Account
    • Contact us
    • Directory
    • Campus Map
    • Support/Give
    • Library Accessibility
      • About SMARTech
      • SMARTech Terms of Use
    Georgia Tech Library266 4th Street NW, Atlanta, GA 30332
    404.894.4500
    • Emergency Information
    • Legal and Privacy Information
    • Human Trafficking Notice
    • Accessibility
    • Accountability
    • Accreditation
    • Employment
    © 2020 Georgia Institute of Technology