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Updated: Jun 15, 2026

Quantitative Analysis and Characterization of Atherosclerotic Lesions in the Murine Aortic Sinus
Published on: December 7, 2013
ADAM33 expression in atherosclerotic lesions and relationship of ADAM33 gene variation with atherosclerosis
John W Holloway1, Ross C Laxton, Matthew J Rose-Zerilli
1Human Genetics, School of Medicine, University of Southampton, and Cardiothoracic Unit, Southampton General Hospital, Southampton, UK.
Abstract:
A-disintegrin-and-metalloproteinase-domains (ADAMs) are membrane-anchored glycoproteins involved in cell adhesion, cell migration and proteolysis. ADAM15 has been implicated in atherosclerosis, with an effect on vascular smooth muscle cell migration. We investigated whether ADAM33, which is evolutionally closely related to ADAM15, was expressed in atheromas and whether it had an effect on vascular smooth muscle migration. We also tested whether ADAM33 gene variation had an influence on the extent of atherosclerosis in patients with coronary artery disease. Immunohistochemical analyses showed that ADAM33 was expressed in smooth muscle cells in the arterial wall and that the expression was increased in smooth muscle cells in atheromas. ADAM33 immunostaining on inflammatory cells in atheromas was also observed. Primary vascular smooth muscle cells in culture were also found to express ADAM33. Boyden chamber assays showed that a neutralising antibody against ADAM33 increased the ability of arterial smooth muscle cells to migrate through a reconstituted basement membrane, suggesting that ADAM33 has an inhibitory effect on vascular smooth muscle migration. Moreover, we detected an association between ADAM33 genotype and the extent of atherosclerosis in a large cohort of coronary artery disease patients. These findings suggest that ADAM33 is implicated in the pathogenesis of atherosclerosis.
Insights
A-disintegrin-and-metalloproteinase-domains 33 (ADAM33) is present in artery walls and atheromas, potentially influencing vascular smooth muscle cell migration. Genetic variations in ADAM33 correlate with atherosclerosis extent in patients.
Area of Science:
- Vascular Biology
- Molecular Medicine
- Cardiovascular Research
Background:
- A-disintegrin-and-metalloproteinase-domains (ADAMs) are key regulators of cell processes.
- ADAM15 is linked to atherosclerosis and vascular smooth muscle cell (VSMC) migration.
- ADAM33, a related protein, warrants investigation in atherosclerosis.
Purpose of the Study:
- To determine ADAM33 expression in atheromas and its effect on VSMC migration.
- To explore the association between ADAM33 gene variations and atherosclerosis severity.
Main Methods:
- Immunohistochemistry to detect ADAM33 expression in arterial walls and atheromas.
- Boyden chamber assays using VSMCs and anti-ADAM33 antibodies.
- Genotyping analysis in a cohort of coronary artery disease patients.
Main Results:
- ADAM33 expression was elevated in VSMCs within atheromas and also found on inflammatory cells.
- Neutralizing antibodies against ADAM33 enhanced VSMC migration, indicating an inhibitory role for ADAM33.
- A significant association was found between ADAM33 genotype and the extent of atherosclerosis.
Conclusions:
- ADAM33 is expressed in the arterial wall and atheromas, with increased levels in atherosclerotic lesions.
- ADAM33 appears to inhibit VSMC migration, suggesting a protective role against excessive cell movement.
- ADAM33 genetic variations are linked to the severity of atherosclerosis, implicating it in disease pathogenesis.
Related Concept Videos
Atherosclerosis I: Introduction
Atherosclerosis III: Management
Atherosclerosis II: Clinical Manifestations and Diagnostic Tests
Peripheral Artery Disease I: Introduction
Coronary Artery Disease I: Introduction
Coronary Artery Disease II: Pathophysiology

