October 1, 1996Circulation
Fluid Flow Inhibits Endothelial Adhesiveness
Key result
Previous exposure to fluid flow decreased cytokine- or lipoprotein-stimulated endothelial cell superoxide production, VCAM-1 expression, and monocyte binding via a nitric oxide-dependent mechanism.
Why the study?
Does fluid flow inhibit endothelial adhesiveness and superoxide production in human aortic endothelial cells exposed to cytokines or oxidized LDL?
Population
Confluent monolayers of human aortic endothelial cells
Comparison
Exposure to fluid flow conditions for 4 hours… vs Static conditions
Design
Preclinical
Follow-up
8 hours (4 hours flow + 4 hours incubation)
Authors
Discussion
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Implication
Supports NO-dependent endothelial protection by flow; hypothesis-generating for regional atheroprotection, needs in vivo confirmation.
Key Points
- This research examines how fluid flow impacts endothelial cell adhesion and its potential protective role against atherogenesis.
- Human aortic endothelial cells were subjected to static or fluid flow for 4 hours.
- Cells were exposed to native LDL, oxidized LDL, or LPS/TNF-alpha for another 4 hours.
- Functional binding assays and superoxide production measurements were conducted following treatments.
- Fluid flow significantly reduced superoxide production and VCAM-1 expression when cells were exposed to inflammatory stimuli (p<0.01).
- Nitric oxide release from flow conditions was confirmed by nitro-L-arginine blockage of these effects.
- PAPA-NONO-ate imitated fluid flow's protective effects, indicating the involvement of NO in reducing endothelial adhesiveness.
Structured PICO
Does fluid flow inhibit endothelial adhesiveness and superoxide production in human aortic endothelial cells exposed to cytokines or oxidized LDL?
P
Population
In vitro study using confluent monolayers of human aortic endothelial cells exposed to static or fluid flow conditions.
I
Intervention
Exposure to fluid flow conditions for 4 hours, followed by incubation with native LDL, oxidized LDL, or LPS + TNF-alpha for 4 hours
C
Comparator
Static conditions
O
Outcome
Endothelial adhesiveness for monocytes, superoxide production, nuclear factor-kappa B activity, and VCAM-1/ICAM-1 expressionsurrogate
Fluid flow inhibits endothelial adhesiveness and superoxide production via shear-induced release of nitric oxide, providing a mechanistic explanation for atheroprotection in regions with normal shear stress.
Cite This Study
Tsao et al. (1996) studied Atherogenesis. Fluid flow vs. Static conditions was evaluated on Superoxide production, nuclear factor-kappa B activity, VCAM-1 expression, and endothelial adhesiveness for monocytes. Previous exposure to fluid flow decreased cytokine- or lipoprotein-stimulated endothelial cell superoxide production, VCAM-1 expression, and monocyte binding via a nitric oxide-dependent mechanism.