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Updated: Jul 20, 2026
05:51
A Human Ex Vivo Atherosclerotic Plaque Model to Study Lesion Biology
Published on: May 6, 2014
Bone morphogenetic protein expression in human atherosclerotic lesions
K Boström1, K E Watson, S Horn
1Division of Cardiology, University of California, Los Angeles School of Medicine 90024-1679.
The Journal of Clinical Investigation
|April 1, 1993
Summary
Artery calcification, a feature of atherosclerosis, may be a regulated bone formation process. Researchers found bone morphogenetic protein-2a and pericyte-like cells in calcified plaques, suggesting these cells mediate arterial calcification.
Area of Science:
- Vascular Biology
- Bone Biology
- Atherosclerosis Research
Background:
- Artery wall calcification in atherosclerosis often contains bone tissue.
- The cellular source of this bone formation within arteries is currently unknown.
Purpose of the Study:
- To investigate the cellular origin of bone formation in atherosclerotic artery walls.
- To determine if arterial calcification is a regulated process akin to bone development.
Main Methods:
- Immunohistochemistry was used to detect bone morphogenetic protein-2a (BMP-2a) in human atherosclerotic plaques.
- Aortic wall cells were cultured to observe calcification and BMP-2a expression.
- Immunocytochemistry identified cell types within cultured calcified nodules.
Main Results:
- Bone morphogenetic protein-2a was expressed in calcified human atherosclerotic plaque.
- Cultured aortic cells formed bone-like calcified nodules and expressed BMP-2a.
- Pericyte-like cells, capable of osteoblastic differentiation, predominated in these nodules and were identified in aortic tissue.
Conclusions:
- Arterial calcification may be a regulated process similar to bone formation.
- Pericyte-like cells in the artery wall are suggested as the mediators of this process.
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