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Adhesion molecules and atherogenesis.

¹Department of Biomedical Engineering, University of Virginia, Health Science Center, Charlottesville, VA 22908, USA.

Acta Physiologica Scandinavica

|October 27, 2001

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Atherosclerosis involves monocyte infiltration, with P-selectin, VLA-4, and VCAM-1 being key adhesion molecules. Blocking these reduces monocyte and lipid accumulation in lesions, suggesting therapeutic potential.

Area of Science:

Cardiovascular Biology
Immunology
Molecular Medicine

Background:

Atherosclerosis is an inflammatory disease driven by monocyte infiltration.
Specific adhesion molecules on endothelial cells and monocytes play critical roles in this process.
Elevated serum levels of soluble adhesion molecules are observed in patients with atherosclerotic diseases.

Purpose of the Study:

To investigate the specific roles of adhesion molecules in monocyte recruitment during atherosclerosis.
To evaluate the therapeutic potential of targeting adhesion pathways in animal models of atherosclerosis.

Main Methods:

In vitro studies using monocytes and cytokine-activated endothelial cells under shear flow.
Ex vivo studies of monocyte adhesion in perfused carotid arteries from atherosclerotic mice (apoE-/-).

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In vivo studies using genetically modified mice (apoE-/-, LDLR-/-) and antibody/peptide blockade of adhesion pathways.

Main Results:

P-selectin and PSGL-1 are crucial for monocyte rolling, while VLA-4 and VCAM-1 mediate firm adhesion.
Genetic deficiency of P-selectin significantly reduced atherosclerotic lesion size in apoE-/- mice.
Blockade of the VLA-4/VCAM-1 pathway reduced monocyte and lipid accumulation in atherosclerotic mouse models.

Conclusions:

P-selectin, PSGL-1, VLA-4, and VCAM-1 are critical for monocyte recruitment in atherosclerosis.
Targeting these adhesion molecules represents a promising therapeutic strategy for atherosclerosis.
Further validation in physiologic models is needed for ICAM-1 and CD18 integrins.