Shear Stress Counteracts Endothelial CX3CL1 Induction and Monocytic Cell Adhesion

Mediators of Inflammation
Aaron BabendreyerAndreas Ludwig

Abstract

Flow conditions critically regulate endothelial cell functions in the vasculature. Reduced shear stress resulting from disturbed blood flow can drive the development of vascular inflammatory lesions. On endothelial cells, the transmembrane chemokine CX3CL1/fractalkine promotes vascular inflammation by functioning as a surface-expressed adhesion molecule and by becoming released as soluble chemoattractant for monocytic cells expressing the receptor CX3CR1. Here, we report that endothelial cells from human artery, vein, or microvasculature constitutively express CX3CL1 when cultured under static conditions. Stimulation with TNFαunder static or very low shear stress conditions strongly upregulates CX3CL1 expression. By contrast, CX3CL1 induction is profoundly reduced when cells are exposed to higher shear stress. When endothelial cells were grown and subsequently stimulated with TNFαunder low shear stress, strong adhesion of monocytic THP-1 cells to endothelial cells was observed. This adhesion was in part mediated by transmembrane CX3CL1 as demonstrated with a neutralizing antibody. By contrast, no CX3CL1-dependent adhesion to stimulated endothelium was observed at high shear stress. Thus, during early stages of vascular inflamma...Continue Reading

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Citations

Jun 5, 2020·Scientific Reports·Mariano A OstuniPhilippe Deterre
Nov 10, 2020·Stroke; a Journal of Cerebral Circulation·Aaron Babendreyer, Andreas Ludwig
Dec 19, 2020·Frontiers in Cardiovascular Medicine·Aaron BabendreyerAndreas Ludwig

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Methods Mentioned

BETA
PCR
flow cytometry

Software Mentioned

IncuCyte ZOOM microscope
SAS
FlowJo
GraphPad
LightCycler®480
PRISM

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