June 26, 2025Open Access

Shear-Induced Macrophage Secretome Promotes Endothelial Permeability

Q: What is the clinical evidence from this study?

Study design: Other. Population: Discrete subaortic stenosis. Intervention: Shear stress and macrophage conditioned media vs. Static conditions (no shear). Primary outcome: Endothelial permeability and inflammatory gene expression.

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Key result

Pathological shear stress induced macrophages to secrete factors that increased endothelial permeability and upregulated inflammatory markers in human aortic endothelial cells.

Why the study?

The impact of hemodynamic shear stress on macrophages and their interactions with endothelial cells in discrete subaortic stenosis remains unclear.

Does pathological shear stress induce macrophages to secrete factors that increase endothelial permeability in an in vitro model?

Population

Human monocyte-derived macrophages and human aortic endothelial cells

Comparison

Shear stress and conditioned media transfer vs baseline conditions

Design

In vitro controlled laboratory study

Authors

EJElysa Jui GKGriffin Kingsley SJSarah Jimenez

Discussion

Member takes

Overview

Hypothesis-generating for shear stress in pediatric DSS recurrence; prospective studies needed before clinical adoption.

Structured PICO

Does pathological shear stress induce macrophages to secrete factors that increase endothelial permeability in an in vitro model?

Population

In vitro study using primary human monocyte-derived macrophages from male donors and human aortic endothelial cells to model the pathophysiology of discrete subaortic stenosis.

Intervention

Uniform laminar shear stress (15 dynes/cm2 and 35 dynes/cm2) applied using a cone-and-plate viscometer for 3 or 24 hours, and exposure to conditioned media (CM) from the opposite cell type.

Comparator

Static conditions (3 hours of no shear) or exposure to the cells' own conditioned media.

Outcome

Cellular crosstalk evaluated through gene expression of inflammatory markers, endothelial permeability, and chemotaxis.surrogate

Pathological shear stress induces macrophages to secrete factors that increase endothelial permeability, suggesting a mechanism for fibrosis and recurrence in discrete subaortic stenosis.

Limitations

In vitro model may not fully replicate in vivo conditions
Specific signaling pathways involved in the crosstalk remain to be identified
Lack of longitudinal in vivo validation
In vitro model lacking in vivo validation
Specific signaling pathways involved in the crosstalk were not fully identified

Cite This Study

Jui et al. (2025) studied Discrete subaortic stenosis. Shear stress and macrophage conditioned media vs. Static conditions (no shear) was evaluated on Endothelial permeability and inflammatory gene expression. Pathological shear stress induced macrophages to secrete factors that increased endothelial permeability and upregulated inflammatory markers in human aortic endothelial cells.

synapsesocial.com/papers/6a7c97cd52489361ef8ce1f4 https://doi.org/10.1101/2025.06.20.660831

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June 26, 2025Open Access

Shear-Induced Macrophage Secretome Promotes Endothelial Permeability

View Full Paper

Ask AI

Bookmark

Key result

Pathological shear stress induced macrophages to secrete factors that increased endothelial permeability and upregulated inflammatory markers in human aortic endothelial cells.

Why the study?

The impact of hemodynamic shear stress on macrophages and their interactions with endothelial cells in discrete subaortic stenosis remains unclear.

Does pathological shear stress induce macrophages to secrete factors that increase endothelial permeability in an in vitro model?

Population

Human monocyte-derived macrophages and human aortic endothelial cells

Comparison

Shear stress and conditioned media transfer vs baseline conditions

Design

In vitro controlled laboratory study

Authors

EJElysa Jui GKGriffin Kingsley SJSarah Jimenez

Discussion

Member takes

Overview

Hypothesis-generating for shear stress in pediatric DSS recurrence; prospective studies needed before clinical adoption.

Structured PICO

Does pathological shear stress induce macrophages to secrete factors that increase endothelial permeability in an in vitro model?

Population

In vitro study using primary human monocyte-derived macrophages from male donors and human aortic endothelial cells to model the pathophysiology of discrete subaortic stenosis.

Intervention

Uniform laminar shear stress (15 dynes/cm2 and 35 dynes/cm2) applied using a cone-and-plate viscometer for 3 or 24 hours, and exposure to conditioned media (CM) from the opposite cell type.

Comparator

Static conditions (3 hours of no shear) or exposure to the cells' own conditioned media.

Outcome

Cellular crosstalk evaluated through gene expression of inflammatory markers, endothelial permeability, and chemotaxis.surrogate

Pathological shear stress induces macrophages to secrete factors that increase endothelial permeability, suggesting a mechanism for fibrosis and recurrence in discrete subaortic stenosis.

Limitations

In vitro model may not fully replicate in vivo conditions
Specific signaling pathways involved in the crosstalk remain to be identified
Lack of longitudinal in vivo validation
In vitro model lacking in vivo validation
Specific signaling pathways involved in the crosstalk were not fully identified

Cite This Study

synapsesocial.com/papers/6a7c97cd52489361ef8ce1f4 https://doi.org/10.1101/2025.06.20.660831

Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

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