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Shear-Induced Macrophage Secretome Promotes Endothelial Permeability.

Elysa Jui, Griffin Kingsley, Sarah Jimenez

    Biorxiv : the Preprint Server for Biology
    |July 16, 2025
    PubMed
    Summary
    This summary is machine-generated.

    Pathological shear stress causes macrophages to increase inflammation and endothelial permeability, contributing to discrete subaortic stenosis (DSS) recurrence. Targeting this macrophage-endothelial cell crosstalk may offer new therapeutic strategies for DSS.

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    Area of Science:

    • Cardiovascular Biology
    • Immunology
    • Pathophysiology

    Background:

    • Discrete subaortic stenosis (DSS) is a pediatric cardiovascular disease characterized by fibrotic growth in the left ventricular outflow tract (LVOT).
    • High recurrence rates post-surgery suggest complex underlying mechanisms involving hemodynamic shear stress.
    • The impact of shear stress on macrophage-endothelial cell interactions in DSS remains poorly understood.

    Purpose of the Study:

    • To investigate the effects of pathological shear stress on human macrophages and their interactions with endothelial cells.
    • To elucidate the role of macrophage-endothelial cell crosstalk in the inflammatory processes relevant to DSS.

    Main Methods:

    • Human monocyte-derived macrophages (MDMs) and human aortic endothelial cells (HAECs) were exposed to shear stress.
    • Cellular responses were assessed via gene expression, permeability assays, chemotaxis, and ELISAs.
    • Macrophage-endothelial cell crosstalk was evaluated using conditioned media transfers.

    Main Results:

    • Shear stress induced a pro-inflammatory response in MDMs, upregulating TNF and CXCL8.
    • MDM-conditioned media increased HAEC permeability and inflammatory marker expression (VCAM-1, ICAM-1).
    • Macrophage-secreted factors promoted monocyte migration and altered endothelial cell junction proteins (VE-Cadherin, CD31).

    Conclusions:

    • Pathological shear stress drives macrophages to release factors that increase endothelial permeability and inflammation.
    • This inflammatory crosstalk likely contributes to fibrosis and recurrence in DSS.
    • Targeting macrophage-endothelial cell interactions presents a potential therapeutic strategy to mitigate DSS fibrosis and improve outcomes.