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Open AccessJournal ArticleDOI

Expression of Extracellular Matrix Proteins Accompanies Lesion Growth in a Model of Intimal Reinjury

Hiroyuki Koyama, +1 more
- 01 May 1998 - 
- Vol. 82, Iss: 9, pp 988-995
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TLDR
It is demonstrated that the accumulation of extracellular matrix is important in the increase in lesion size after reinjury and that a balance of matrix synthesis and degradation may explain why no change in matrix volume was detected until 28 days after the reinjury.
Abstract
—Reinjury of rat arterial lesions induces an increase in lesion size that is not associated with an increase in cell number. In this study, matrix volume was examined after reinjury to preexisting lesions, and the kinetics of matrix gene expression and activity of proteolytic enzymes in the lesion were evaluated. Volume densitometry in intima showed a significant increase in matrix volume 28 days after the reinjury, although no change was observed at 14 days. Three common vascular matrix molecules, α1(I)procollagen, tropoelastin, and fibronectin, were expressed highly at 7 days after the reinjury. Expression of tropoelastin remained upregulated for the entire 28 days after the reinjury, whereas α1(I)procollagen and fibronectin returned to the control level by 28 days. Protease activity was also increased after reinjury. Within days, a marked increase in urokinase plasminogen activator activity was observed in intima, and this activity decreased to control level by 14 days. The activity of tissue p...

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Citations
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TL;DR: This review discusses cellular sources of collagen synthesis in atherosclerosis, local and systemic factors modulating collagen gene expression, as well as temporal and spatial patterns of collagen production in human and experimental atherosclerotic lesions.
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Inhibition of miR-92a improves re-endothelialization and prevents neointima formation following vascular injury.

TL;DR: It is indicated that inhibition of endothelial miR-92a attenuates neointimal lesion formation by accelerating re-endothelialization and thus represents a putative novel mechanism to enhance the functional recovery following vascular injury.
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Vein wall remodeling after deep vein thrombosis involves matrix metalloproteinases and late fibrosis in a mouse model

TL;DR: In this article, the expression of proteases and collagen involved in early vein wall remodeling was investigated in early venous thrombosis in the mouse, and the results showed that wound healing after DVT is similar to wound healing and is associated with increased procollagen gene expression and total collagen.
References
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Journal ArticleDOI

Expression of Matrix Metalloproteinases and Their Inhibitor TIMP-1 in the Rat Carotid Artery After Balloon Injury

TL;DR: The results demonstrate that the process of extracellular matrix breakdown by MMPs after balloon catheter-induced injury is controlled by a tightly regulated temporal response by the genes responsible for the production of these enzymes and their inhibitor and by post-translational activation of the proenzymes.
Journal ArticleDOI

Homology cloning of rat 72 kDa type IV collagenase: cytokine and second-messenger inducibility in glomerular mesangial cells.

TL;DR: It is concluded that Cytokine and second-messenger inducibility may contribute to the enhanced expression of the enzyme during glomerular inflammatory disorders.
Journal ArticleDOI

Characteristics of a 95-kda matrix metalloproteinase produced by mammary carcinoma cells

TL;DR: This suggests that expression of the Mr 95,000 MMP is regulated differently from that of interstitial collagenase, which is produced by the epithelial cells only in response to specific inductive factor(s) from the myoepithelial-like cells.
Journal ArticleDOI

Plasminogen Activator Inhibitor Type 1 and Tissue Inhibitor of Metalloproteinases-2 Increase After Arterial Injury in Rats

TL;DR: The increase of PAI-1 and TIMP-2 after injury supports the hypothesis that changes in the proteolytic balance play an important role in smooth muscle cell migration after arterial injury.
Journal ArticleDOI

Co-operation between plasmin and elastase in elastin degradation by intact murine macrophages.

TL;DR: The results indicate that live macrophage elastinolysis is a co-operative process involving multiple proteinases, especially a cysteine proteinase(s) and elastase, and plasmin may be a physiological activator of latent macrophages or cell-free elast enzyme-rich medium.
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These findings demonstrate that the accumulation of extracellular matrix is important in the increase in lesion size after reinjury and that a balance of matrix synthesis and degradation may explain why no change in matrix volume was detected until 28 days after the reinjury.