1996

DOI: 10.1016/s0268-9499(96)80043-9

|View full text |Cite

|

Sign up to set email alerts

|

The role of plasminogen activators in the development of atherosclerotic and restenotic lesions

¹

,

²

,

³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Discussion3

Introduction2

Citation Types

Supporting

0

Mentioning

5

Contrasting

0

Year Published

1998

1998

2003

2003

Publication Types

Select...

Article6

Relationship

Self Cite0

Independent6

Authors

Journals

Cited by 6 publications

(5 citation statements)

References 15 publications

Supporting

0

Mentioning

5

Contrasting

0

Order By: Relevance

“…Evidence from experiments of injured rat arteries and development of atherosclerotic and restenotic lesions have shown the positive correlation between the expression of plasminogen activators tPA and uPA and the migration of SM cells into the intima (16,19). In addition, plasmin may activate MMPs (17) to augment adventitial extracellular proteolysis.…”

Section: Discussionmentioning

confidence: 99%

Remodeling of the adventitia during coronary arteriogenesis

¹

,

²

,

³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

We studied the role of the adventitia in adaptive arteriogenesis during the phase of active growth of coronary collateral vessels (CV) induced by chronic occlusion of the left circumflex coronary artery in canine hearts. We used electron microscopy and immunoconfocal (IF) labeling for bFGF, matrix metalloproteinase (MMP)-2, MMP-9, tissue-type plasminogen activator (tPA), its inhibitor (PAI-1), fibronectin (FN), and Ki-67. Proliferation of smooth muscle cells and adventitial fibroblasts was evident. Quantitative IF showed that adventitial MMP-2, MMP-9, and FN were 9.2-, 7.5-, and 8.6-fold, bFGF was 5.1-fold, and PAI-1 was 3.4-fold higher in CV than in normal vessels (NV). The number of fibroblasts was 5-fold elevated in CV, but the elastic fiber content was 25-fold greater in NV than in CV. Perivascular myocyte damage and induction of endothelial nitric oxide synthase in peri-CV capillaries indicate expansion of CV. It was concluded that adventitial activation is associated with the development of CV through cell proliferation, production of growth factors, and induction of extracellular proteolysis thereby contributing to remodeling during adaptive arteriogenesis. collateral vessel growth; metalloproteinases; extracellular proteolysis; dog CORONARY COLLATERAL VESSEL GROWTH in the dog heart, induced by chronic occlusion of a major coronary artery, results in a 20-50 times increase in diameter (21). The mechanism of collateral vessel growth is only partially understood. Many factors or events have been indicated to make contributions to this process, e.g., increased shear stress, early invasion of monocytes/ macrophages, reexpression of fetal proteins, extracellular proteolysis, migration of smooth muscle (SM) cells, and involvement of gap junction proteins (3,4,29). The notion that apoptosis of SM cells, fibroblasts, or myocytes creates space for the enlargement of collateral vessels has also been proposed (23). These studies addressed the crucial role of endothelium and of SM cells in the development of coronary collateral vessels.However, the importance of the tunica adventitia in vascular remodeling was largely neglected, although enlargement of collateral vessels without participation of the adventitia seems not conceivable. We hypothesize that the adventitia is activated and might be an important contributor to the development of coronary collaterals.The development of coronary collateral vessels has been classified into three phases: early growth (2-3 wk postsurgery), active growth (4-6 wk postsurgery), and maturation (8-12 wk postsurgery) (4). An early study showed that an acute inflammatory reaction was present in the adventitia of collateral vessels in the phase of early growth (2). However, in the phases of active growth and maturation, inflammatory cells have not been observed in the adventitia, and fibroblasts are the predominant cells residing in the adventitia. Fibroblasts have been demonstrated to be active participants in vascular remodeling (20,25,26). Here, we studied the question whether typica...

“…Evidence from experiments of injured rat arteries and development of atherosclerotic and restenotic lesions have shown the positive correlation between the expression of plasminogen activators tPA and uPA and the migration of SM cells into the intima (16,19). In addition, plasmin may activate MMPs (17) to augment adventitial extracellular proteolysis.…”

Section: Discussionmentioning

confidence: 99%

Remodeling of the adventitia during coronary arteriogenesis

¹

,

²

,

³

et al. 2003

American Journal of Physiology-Heart and Circulatory Physiology

View full text Add to dashboard Cite

We studied the role of the adventitia in adaptive arteriogenesis during the phase of active growth of coronary collateral vessels (CV) induced by chronic occlusion of the left circumflex coronary artery in canine hearts. We used electron microscopy and immunoconfocal (IF) labeling for bFGF, matrix metalloproteinase (MMP)-2, MMP-9, tissue-type plasminogen activator (tPA), its inhibitor (PAI-1), fibronectin (FN), and Ki-67. Proliferation of smooth muscle cells and adventitial fibroblasts was evident. Quantitative IF showed that adventitial MMP-2, MMP-9, and FN were 9.2-, 7.5-, and 8.6-fold, bFGF was 5.1-fold, and PAI-1 was 3.4-fold higher in CV than in normal vessels (NV). The number of fibroblasts was 5-fold elevated in CV, but the elastic fiber content was 25-fold greater in NV than in CV. Perivascular myocyte damage and induction of endothelial nitric oxide synthase in peri-CV capillaries indicate expansion of CV. It was concluded that adventitial activation is associated with the development of CV through cell proliferation, production of growth factors, and induction of extracellular proteolysis thereby contributing to remodeling during adaptive arteriogenesis. collateral vessel growth; metalloproteinases; extracellular proteolysis; dog CORONARY COLLATERAL VESSEL GROWTH in the dog heart, induced by chronic occlusion of a major coronary artery, results in a 20-50 times increase in diameter (21). The mechanism of collateral vessel growth is only partially understood. Many factors or events have been indicated to make contributions to this process, e.g., increased shear stress, early invasion of monocytes/ macrophages, reexpression of fetal proteins, extracellular proteolysis, migration of smooth muscle (SM) cells, and involvement of gap junction proteins (3,4,29). The notion that apoptosis of SM cells, fibroblasts, or myocytes creates space for the enlargement of collateral vessels has also been proposed (23). These studies addressed the crucial role of endothelium and of SM cells in the development of coronary collateral vessels.However, the importance of the tunica adventitia in vascular remodeling was largely neglected, although enlargement of collateral vessels without participation of the adventitia seems not conceivable. We hypothesize that the adventitia is activated and might be an important contributor to the development of coronary collaterals.The development of coronary collateral vessels has been classified into three phases: early growth (2-3 wk postsurgery), active growth (4-6 wk postsurgery), and maturation (8-12 wk postsurgery) (4). An early study showed that an acute inflammatory reaction was present in the adventitia of collateral vessels in the phase of early growth (2). However, in the phases of active growth and maturation, inflammatory cells have not been observed in the adventitia, and fibroblasts are the predominant cells residing in the adventitia. Fibroblasts have been demonstrated to be active participants in vascular remodeling (20,25,26). Here, we studied the question whether typica...

“…In addition to its important protective function against stable thrombus formation, the PA system also plays a role in the development of atherosclerosis 3 , 5 , 28 . Enhanced expression of PAI‐1, tPA, uPA and uPAR has been reported in the endothelium, the media and the intima of human coronary atherosclerotic arteries 3 , 5 , 29 . Of these four components of the PA system, the increase in PAI‐1 expression is most predominant.…”

Section: Discussionmentioning

confidence: 99%

“…Of these four components of the PA system, the increase in PAI‐1 expression is most predominant. Such overexpression of PAI‐1 can be associated with thrombus formation and represents a risk for acute coronary thrombosis 3 , 5 , 28 , 29 . Increased tPA, uPA and uPAR expression may also promote monocyte and smooth muscle cell migration, thereby facilitating proteolytic weakening of plaques 3 , 5 , 28 , 29 …”

Section: Discussionmentioning

confidence: 99%

“…Ischaemic heart disease is frequently coupled with coronary atherosclerosis and the rupture of atherosclerotic plaques with superimposed thrombosis is a major cause for acute events in coronary artery disease 1 . The development of ischaemic heart disease is accompanied by a reduced fibrinolytic capacity 2 , 3 . Reduced fibrinolysis may also be involved in the progression of atherosclerosis 4 –6 .…”

Section: Introductionmentioning

confidence: 99%

“…In atherosclerotic lesions within coronary arteries, monocytes also participate in lipid and cell debris removal as well as regulating inflammation 3 , 5 . Here, their initial adhesion to endothelium and migration into the vessel wall is associated with the expression of the β2‐integrins CD11b/CD18; 19 this complex (Mac‐1) plays a pivotal role in monocyte adhesion to damaged endothelium 20 , 21 …”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Urokinase Plasminogen Activator System in Humans With Stable Coronary Artery Disease

Красникова

¹

,

²

,

Алексеева

³

et al. 1999

Clin Exp Pharma Physio

View full text Add to dashboard Cite

1. The present study compares plasma urokinase plasminogen activator (uPA) peptide levels, plasma plasminogen inhibitor (PAI-1) activity and urokinase receptors (uPAR) on peripheral blood monocytes of patients with stable coronary artery disease (SCAD) and healthy volunteers. 2. Urokinase plasminogen activator levels were analysed by ELISA and PAI-1 activity was determined by a plasmin generation method using the chromogenic substrate S2390. Relative uPAR numbers and the adhesion molecules CD11b/CD18 on peripheral blood monocytes were estimated using specific antibodies and flow cytometry. 3. Patients with SCAD were found to have higher plasma uPA peptide levels than age-matched healthy subjects (10.40 +/- 0.99 vs 8.25 +/- 0.53 pmol/L, respectively; P < 0.05). 4. Plasma PAI-1 activity was also higher in patients with SCAD than in healthy subjects (13.6 +/- 2.5 vs 5.2 +/- 1.0 IU/mL, respectively; P < 0.05). 5. Relative uPAR and CD11b/CD18 adhesion molecules were similar on peripheral blood monocytes of patients with SCAD and in healthy subjects. 6. The data indicate a pattern of expression/activity of uPA and PAI-1 in patients with SCAD suggestive of an impaired fibrinolytic ability.

The urokinase receptor mediates basic fibroblast growth factor-dependent smooth muscle cell migration through baboon aortic explants

¹

,

²

,

³

2002

Atherosclerosis

View full text Add to dashboard Cite

No abstract

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Product

Browser Extension Assistant by scite Citation Statement Search Reference Check Visualizations Dashboards Explore Journals Explore Organizations Explore Funders Embedding Badge Embedding Citation Search Pricing

Resources

Blog Help & FAQ Accessibility Statement API Terms For Universities & Governments For Researchers For Publishers For Corporate, Pharma & Enterprise Author Marketing Become an Affiliate Get an organization trial or quote scite Data & Services

About

News & Press Careers Read our Paper Coverage

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Copyright © 2025 scite LLC. All rights reserved.

Made with 💙 for researchers

Part of the Research Solutions Family.