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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
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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Collagen synthesis in atherosclerosis: too much and not enough.

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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Collagens and atherosclerosis.

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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 Article

Kinetics of cellular proliferation after arterial injury. I. Smooth muscle growth in the absence of endothelium.

TL;DR: The concept that intimal SMC proliferation after arterial injury is an acute event related to the initial injury process is supported, as persistent proliferation of luminal SMC does not result in an increase in intimal cell number.
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Inhibition of Neointimal Smooth Muscle Accumulation After Angioplasty by an Antibody to PDGF

TL;DR: It is demonstrated that endogenous PDGF is involved in the accumulation of neointimal smooth muscle cells associated with balloon injury and may be involved in restenosis after angioplasty, and perhaps in atherogenesis as well.
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Restenosis After Successful Percutaneous Transluminal Coronary Angioplasty: Serial Angiographic Follow-Up of 229 Patients

TL;DR: Restenosis is most prevalent between 1 and 3 months and rarely occurs beyond 3 months after coronary angioplasty and reached a plateau thereafter.
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Mechanism of activation of latent recombinant transforming growth factor beta 1 by plasmin.

TL;DR: Chemical cross-linking of CHO-conditioned medium and immunoblot analyses indicates that latent recombinant TGF beta 1 contains both the cleaved amino-terminal glycopeptide and mature TGFbeta 1 polypeptide in a noncovalent association and that this association confers latency.
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Three different fibronectin mRNAs arise by alternative splicing within the coding region.

TL;DR: There are at least three different fibronectin mRNAs in rat liver which differ in coding potential and are probably all encoded by a single gene, according to the sequence data and S1 nuclease mapping.
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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.