Document Detail


Temporal and quantitative analysis of expression of metalloproteinases (MMPs) and their endogenous inhibitors in atherosclerotic lesions.
MedLine Citation:
PMID:  18830936     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Matrix metalloproteinases (MMPs) play an important role in the pathogenesis of vascular diseases, such as atherosclerosis, plaque rupture and aneurysms. Although several MMPs have been demonstrated in the lesions of atherosclerosis, their expression profiles during the initiation and progression of lesions have not been fully determined. We hypothesized that the expression of various MMPs, along with their endogenous inhibitors, may be differentially regulated dependent upon the lesion progression. Therefore, we made a temporal and quantitative analysis of the mRNA and protein expression of MMPs and tissue inhibitors of metalloproteinases expressed in the different stages of atherosclerotic lesions of rabbits and humans. We found that MMP-1, MMP-12 and MMP-13 expression was nearly absent in the normal arterial wall, but was remarkably increased with lesion progression. Furthermore, the expression of these MMPs in the lesions was closely associated with intimal macrophages and monocyte chemoattractant protein-1 expression, suggesting that the intimal macrophages are the major source of production of these MMPs. MMP-3 and MT1-MMP were also significantly upregulated in the early-stage lesions and fatty streaks compared to the normal aortas of rabbits. Our results indicate that MMP-1, -12, and -13 derived from intimal macrophages may play a pivotal role in both lesion initiation and progression, and therefore are potential therapeutic targets for the treatment of plaque rupture and aneurysm formation.
Authors:
Ying Yu; Tomonari Koike; Shuji Kitajima; Enqi Liu; Masatoshi Morimoto; Masashi Shiomi; Kinta Hatakeyama; Yujiro Asada; Ke-Yong Wang; Yasuyuki Sasaguri; Teruo Watanabe; Jianglin Fan
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Histology and histopathology     Volume:  23     ISSN:  1699-5848     ISO Abbreviation:  Histol. Histopathol.     Publication Date:  2008 Dec 
Date Detail:
Created Date:  2008-10-02     Completed Date:  2008-12-30     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8609357     Medline TA:  Histol Histopathol     Country:  Spain    
Other Details:
Languages:  eng     Pagination:  1503-16     Citation Subset:  IM    
Affiliation:
Department of Molecular Pathology, Interdisciplinary Graduate School of Medicine and Engineering, University of Yamanashi, Yamanashi, Japan.
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MeSH Terms
Descriptor/Qualifier:
Animals
Aorta / metabolism,  pathology
Atherosclerosis / genetics,  metabolism*,  pathology*
Blotting, Western
Chemokine CCL2 / biosynthesis
Disease Progression
Gene Expression
Gene Expression Profiling
Humans
Immunohistochemistry
Macrophages / metabolism
Male
Metalloproteases / biosynthesis*,  genetics
RNA, Messenger / analysis
Rabbits
Reverse Transcriptase Polymerase Chain Reaction
Tissue Inhibitor of Metalloproteinases / biosynthesis*,  genetics
Tunica Intima / cytology
Chemical
Reg. No./Substance:
0/CCL2 protein, human; 0/Chemokine CCL2; 0/RNA, Messenger; 0/Tissue Inhibitor of Metalloproteinases; EC 3.4.-/Metalloproteases

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