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Updated: Mar 25, 2026

Investigating Aortic Valve Calcification via Isolation and Culture of T Lymphocytes using Feeder Cells from Irradiated Buffy Coat
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C4b-Binding Protein Deposition is Induced in Diseased Aortic Heart Valves, Coinciding with C3d

Maria Jose Dikhoff, Mimi ter Weeme, Alexander B A Vonk

    The Journal of Heart Valve Disease
    |February 23, 2016
    PubMed

    Insights

    C4b-binding protein (C4BP) is deposited in diseased aortic valves, correlating with complement activation marker C3d. C4BP levels were highest in infected atherosclerotic valves, exceeding other complement inhibitors.

    Area of Science:

    • Immunology
    • Cardiovascular Pathology
    • Complement System

    Background:

    • Activated complement is prevalent in diseased aortic valves.
    • Endogenous complement inhibitors C1-inhibitor and clusterin are less abundant than activated complement.
    • C4b-binding protein (C4BP) is an endogenous complement inhibitor found in diseased coronary arteries.

    Purpose of the Study:

    • To investigate the levels of C4b-binding protein (C4BP) in diseased aortic valves.
    • To compare C4BP deposition in different types of diseased aortic valves.

    Main Methods:

    • Aortic valve tissues were classified as degenerative, atherosclerotic, or atherosclerotic with bacterial infection.
    • Immunohistochemical staining was performed for C4BP, C3d, and caspase-3.
    • Computer-assisted morphometry quantified positive staining areas.

    Main Results:

    • C4BP and C3d deposition was significantly higher in atherosclerotic valves compared to degenerative and control groups.
    • Atherosclerotic valves with bacterial infection showed further increased C4BP and C3d positivity.
    • Caspase-3 was detected in a small percentage of endothelial cells and neutrophils.

    Conclusions:

    • C4b-binding protein (C4BP) is deposited in diseased aortic valves, co-localizing with C3d.
    • C4BP deposition in diseased aortic valves is more extensive than other endogenous complement inhibitors.
    • Findings suggest a role for C4BP in aortic valve disease pathogenesis.
    Abstract

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