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Cardiovascular Engineering

Cardiovascular Engineering - Poster Session E

T2 - Lipidomic Profiling Reveals Ceramide-Associated Caveolin-1 Migration in Vascular Calcification

Saturday, October 11, 2025
10:00 AM - 11:00 AM PDT
Location: Exhibit Hall F, G & H

    Presenting Author(s)

  • SB

    Stephania Barroso Avila

    Undergraduate Student Researcher
    Cardiovascular Matrix Remodeling Lab
    Hialeah, Florida, United States

    • Co-Author(s)

  • KK

    Katherine Kaiser

    PhD Candidate
    Florida International University
    Miami, Florida, United States

    • Primary Investigator(s)

  • Joshua D. Hutcheson

    Associate Professor
    Florida International University
    Miami, Florida, United States

    • Co-Author(s)

  • FF

    Francisco A. Fernandez-Lima

    Professor
    Florida International University, Florida, United States


Introduction: : Calcification in Vascular Smooth Muscle Cells (VSMCs) is the process of deposition of calcium within the arterial walls, which can result in cardiovascular morbidity and mortality. Preliminary results indicate that ceramides co-localize with Caveolin-1 (Cav1) during the mineralization process. Ceramide accumulation in lipid rafts has previously been shown to displace cholesterol and facilitate dissociation of Cav1 from these membrane regions.

Materials and

Methods: : The Cav1 protein regulates calcium deposition from VSMC cells by influencing the formation of calcific extracellular vesicles (EVs). CAV1 has previously been observed to migrate from low-density caveolar membrane regions to unknown heavier-density membrane fractions during vascular calcification (VC), as determined by density gradient ultracentrifugation. However, the key mediators of this density change remain unidentified.To explore this, we conducted unbiased lipidomic analysis of each membrane fraction in pro-calcific and control conditions to identify interactions with CAV1 that contribute to this observed change in density.

Results, Conclusions, and Discussions:: Furthermore, inhibition of SMPD3, a ceramide-producing enzyme, has been shown to reduce calcification in vitro through prevention of EV formation. We hypothesize that the association of ceramides, under calcifying conditions, promotes CAV1 translocation, potentially acting as an upstream regulator of VC development. This connection between CAV1 trafficking and the membrane lipid remodeling provides new insight into the essential role of lipid metabolism and lipid-protein interactions in VC.

Acknowledgements and/or References (Optional): : Stephania Barroso*, Katherine Kaiser, Dr. Francisco Alberto Fernandez-Lima, Dr. Joshua D. Hutcheson.
Department of Biomedical Engineering, College of Engineering, Florida International University, Miami, Florida, 33199