期刊
BIOMECHANICS AND MODELING IN MECHANOBIOLOGY
卷 8, 期 6, 页码 473-486出版社
SPRINGER HEIDELBERG
DOI: 10.1007/s10237-009-0151-8
关键词
Atherosclerosis; Plaque progression; Plaque rupture; Nuclear factor-kappa B; Matrix metalloproteinase; Macrophages; Heterogeneous finite element model; Mechanobiology; Mechanical stress
资金
- National Institute of Health [RO1HL070531]
In this study, we hypothesized that spatial relationships exist between the local mechanical environment and inflammatory marker expression in atherosclerotic plaques, and that these relationships are plaque-progression dependent. Histologic cross-sections were collected at regular intervals along the length of diseased human coronary arteries and classified as early, intermediate, advanced, or mature based on their morphological features. For each cross-section, the spatial distribution of stress was determined using a 2D heterogeneous finite element model, and the corresponding distribution of selected inflammatory markers (macrophages, matrix metalloproteinase-1 [MMP-1], and nuclear factor-kappa B [NF-kappa B]) were determined immunohistochemically. We found a monotonic spatial relationship between mechanical stress and activated NF-kappa B that was consistent in all stages of plaque progression. We also identified progression-dependent relationships between stress and both macrophage presence and MMP-1 expression. These findings add to our understanding of the role of mechanical stress in stimulating the inflammatory response, and help explain how mechanical factors may regulate complex biological changes in remodeling.
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