Adhesion molecules, chemokines and oxidative stress in atherosclerosis

The role of different stimuli recognized to play an important part in atherosclerosis development (chemokines, cytokines, oxidized lipoproteins) on leukocyte adhesion to endothelial cells or purified adhesion molecules, under physiological flow conditions are investigated.
The main focus was on leukocyte adhesion to Fractalkine or VCAM-1, triggered by cytokines like TNFα or IFNγ, and by chemokines such as MCP-1. Inhibition profiles were also generated, blocking the specific binding to VCAM-1 using an anti-α4 mAb on THP-1 monocytic cell line, or interfering on the binding between fractalkine and its receptor CX3CR1 on PBMCs with the soluble form of the chemokine.
OxLDL has also been shown to upregulate the expression of adhesion molecules, as assessed through flow cytometric analysis, resulting in an increased adhesion of monocytes to endothelial cells under flow conditions.

In motion


Inflammation - Atherosclerosis
THP-1 monocytes adhering to HUVECs in biochip under flow


Primary monocyte adhesion to coronary artery endothelium under shear flow

Inflammation - Atherosclerosis:
Tracking of THP-1 monocytes rolling on E-selectin coated biochip


Leukocyte Rollling of THP-1 monocytes on E-selectin coated microchannel at 0.5 dyne/cm²


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