The expression of matrix metalloproteinases-9, transforming growth factor-β1 and transforming growth factor-β receptorⅠ in human atherosclerotic plaque and their relationship with plaque stability

被引:13
作者
姜昕
曾和松
郭毅
周志斌
唐冰杉
李富康
机构
[1] Department of Cardiology
[2] Tongji Hospital
[3] Tongji Medical College
[4] Huazhong University of Science and Technology
[5] Wuhan
[6] China
[7] Department of Neurology
[8] Second Affiliated Hospital of Jinan University
[9] Shenzhen
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D O I
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中图分类号
R543.5 [动脉疾病];
学科分类号
1002 ; 100201 ;
摘要
Background Transforming growth factor beta (TGF β) and matrix metalloproteinases 9 (MMP 9) have been implicated in the pathogenesis of human atherosclerosis but their relationship during lesion progression are poorly understood The objective of this study was to investigate the expression of MMP 9, TGF β1 and TGF β receptor Ⅰ (TβR Ⅰ) in human atherosclerotic plaque and their relationship and plaque stability Methods Specimens of human coronary artery atherosclerotic plaques were obtained from 41 patients undergoing coronary endarterectomy, and were paraffin embedded, sectioned at 4 μm intervals then stained with haematoxylin and eosin They were divided into stable (with no or only little lipid core) and unstable plaque groups (with lipid core size>40%): the immunohistochemical staining were performed for MMP 9,TGF β1 and TβR Ⅰ Results The expression of MMP 9 in the unstable plaques was much higher than in the stable ones, but the expression of TGF β1 was higher in the stable plaques There was no similar significant difference for TβR Ⅰ Correlation analysis showed that there was a negative correlation between the expression of MMP 9 and TGF β1 ( r =-0 332, P =0 034 for average areal density; r =-0 373, P = 0 016 for average optical density) Conclusions There were close relationships between MMP 9, TGF β1 and plaque stability Enhanced production of MMP 9 may participate in the formation of unstable plaque, while TGF β1 maybe an important stabilizing factor in preventing transition into an unstable plaque phenotype
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