| Extracellular matrix collagen synthesis and degradation following coronary balloon angioplasty. | |
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MedLine Citation:
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PMID: 8732498 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Percutaneous transluminal coronary angioplasty is associated with intimal hyperplasia and extracellular matrix deposition of collagen, leading to restenosis in a significant number of cases. The purpose of the present study was to determine the effects of balloon angioplasty on extracellular matrix collagen content and collagenase activity in a porcine coronary artery restenosis model 6 weeks following balloon injury. We tested the hypothesis that in balloon-injured arteries the neointimal extracellular matrix was characterized by increased collagen content and decreased metalloproteinase activity relative to non-injured arteries. Male miniswine maintained on a high cholesterol diet underwent cardiac catheterization and double balloon injury to the right and left circumflex coronary arteries. The coronary arteries were either pressure-perfusion-fixed and prepared for histological examination, or dissected free of adventitia for further collagen and matrix metalloproteinase studies. Collagen synthesis in balloon-injured coronary arteries was compared to non-injured arteries using Northern blot analysis and histochemical stains. Comparative studies on differences between balloon-injured and non-balloon-injured arterial matrix metalloproteinase activity were done using zymography. Balloon angioplasty arterial injury resulted in a significant increase in type I collagen mRNA expression, with increased collagen deposition in the extracellular matrix. In contrast, matrix metalloproteinase activity was markedly decreased. The results suggest that the increased neointimal extracellular matrix observed late in the injury response may be due to not only increased collagen synthesis, but also reduced degradation. The failure to achieve a balance between the synthesis and degradation of extracellular matrix collagen could serve as an important mechanism responsible for restenosis. |
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Authors:
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E Guarda; L C Katwa; S E Campbell; M A Tanner; R M Webel; H Laughlin; S Jenkins; P R Myers |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Journal of molecular and cellular cardiology Volume: 28 ISSN: 0022-2828 ISO Abbreviation: J. Mol. Cell. Cardiol. Publication Date: 1996 Apr |
Date Detail:
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Created Date: 1996-11-12 Completed Date: 1996-11-12 Revised Date: 2006-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0262322 Medline TA: J Mol Cell Cardiol Country: ENGLAND |
Other Details:
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Languages: eng Pagination: 699-706 Citation Subset: IM |
Affiliation:
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Depto. Enfermedades Cardiovasculares, Hospital Clinico, Universidad Catolica de Chile, Santiago. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Angioplasty, Transluminal, Percutaneous Coronary
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adverse effects* Animals Blotting, Northern Collagen / biosynthesis, metabolism* Collagenases / metabolism Coronary Disease / metabolism, therapy* Coronary Vessels / enzymology, metabolism Extracellular Matrix Proteins / biosynthesis, metabolism* Male RNA, Messenger / analysis Recurrence Swine |
| Chemical | |
Reg. No./Substance:
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0/Extracellular Matrix Proteins; 0/RNA, Messenger; 9007-34-5/Collagen; EC 3.4.24.-/Collagenases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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