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Updated: Jun 23, 2026
05:51
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Integrin and matrix metalloproteinase expression in human carotid plaque
Carlos A Murillo1, Kenneth J Woodside, Qian Guo
1Department of Surgery, University of Texas Medical Branch, Galveston, Texas, USA.
The Journal of Surgical Research
|April 28, 2009
Summary
Restenotic lesions after carotid procedures show decreased integrin expression and protease activity, indicating a quiescent phase. This highlights the role of proteinase/inhibitor imbalance in plaque remodeling.
Area of Science:
- Cardiovascular Biology
- Vascular Biology
- Atherosclerosis Research
Background:
- Neointimal thickening drives restenosis post-carotid endarterectomy (CEA) and stenting.
- Smooth muscle cells (SMCs), endothelial cells (ECs), and extracellular matrix (ECM) interactions regulate lesion biology.
- The role of ECM proteins in neointimal lesion remodeling remains less defined compared to cellular components.
Purpose of the Study:
- To investigate the role of extracellular matrix (ECM) proteins in neointimal lesion remodeling after carotid interventions.
- To compare the molecular characteristics of primary atherosclerotic plaques and restenotic lesions following carotid endarterectomy (CEA).
Main Methods:
- Analysis of primary and restenotic carotid endarterectomy specimens.
- Western immunoblotting for protein extraction, RT-PCR, and cDNA microarray analysis for gene expression.
- Zymography to assess protease activity.
Main Results:
- Microarray identified altered expression of 13 genes between primary and restenotic lesions.
- Primary plaques showed higher expression of alpha2-, alpha6-, and beta3-integrin genes compared to restenotic lesions.
- Increased protein expression of plasminogen activator inhibitor-1 (PAI-1) and tissue inhibitor of metalloproteinase (TIMP-1) was observed in primary plaques, along with elevated pro-MMP-2, pro-MMP-9 levels, and MMP-2 activity.
Conclusions:
- Restenotic lesions exhibit decreased integrin expression and protease activity, suggesting a quiescent state.
- Imbalances in proteinase and inhibitor expression are crucial in regulating neointimal plaque remodeling.
- Findings underscore the importance of ECM protein dynamics in post-carotid intervention restenosis.
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