Aim To investigate the expression of matrix metalloproteinases-9 (MMP-9), transforming growth factor-beta1 (TGF-β1) and TGF-beta receptorⅠ (TβR-Ⅰ)in human atherosclerotic plaque and the relationship between them and plaque stability. Methods 41 specimen of human coronary artery atherosclerotic plaque were obtained from patients undergoing cardiovascular surgery, and then were routine paraffin embedded, sectioned at 4 μm, and stained with hematoxylin and eosin. They were divided into stable (with no or only little lipid core) and unstable plaques (with lipid core size >40%) according to the structure under the opticalmicroscope, the qualitive and quantitive analyses of MMP-9, TGF-β1 and TβR-Ⅰ were performed by using immunohistochemical staining technique and auto picture analysis system. Results The immunopositive stain of MMP-9, TGF-β1 and TβR-Ⅰwere all located in the vascular smooth muscle cells, endothelial cells, fibroblast, and particularly in the foam cells and macrophage in the atherosclerotic plaque tissue. The protein expression of MMP-9 in the unstable plaques was much stronger than that in the stable ones (average area density: 0.21±0.04 vs 0.16±0.02, average absorbent values: 3.48±0.65 vs 2.84± 0.27 , p<0.01), and was also stronger on the shoulder of the plaque, in the foam cells and macrophage around the lipid core, while the protein expression of TGF-β1 was much stronger in the stable plaques (average area density: 0.23±0.05 vs 0.17± 0.02 , p<0.01; average absorbent values: 3.60±0.55 vs 3.16±0.65, p<0.05). There were no significant difference for immunopositive stain of TβR-Ⅰbetween the stable and unstable plaques. Correlation analysis showed that there was a negative correlation between the expression of MMP-9 and TGF-β1 with both average area density and average absorbent values (r= -0.332 , P=0.034 for average area density; r=-0.373, P=0.016 for average absorbent values). Conclusions There was a close relationship between MMP-9,TGF-β1 and plaque stability. Enhanced production MMP-9 may participate in the formation of unstable plaque, while TGF-β1 may be an important stabilizing factor to prevent the transition into an unstable plaque phenotype.