Remodeling of carotid artery is associated with increased expression of matrix metalloproteinases in mouse blood flow cessation model

Circulation

Volumn 102, Issue 23, 2000, Pages 2861-2866

  Godin, D ^a   Ivan, E ^a   Johnson, C ^a   Magid, R ^a   Galis, Z S ^a  

^a EMORY UNIVERSITY SCHOOL OF MEDICINE   (United States)

Author keywords

Carotid arteries; Metalloproteinases; Remodeling

Indexed keywords

ANIMAL MODEL; ANIMAL TISSUE; ARTERY INTIMA PROLIFERATION; ARTICLE; ATHEROSCLEROSIS; CAROTID ARTERY FLOW; CAROTID ARTERY OBSTRUCTION; CELL MIGRATION; ENZYME ACTIVITY; MALE; MOUSE; NONHUMAN; PRIORITY JOURNAL; PROTEIN EXPRESSION; RESTENOSIS;

EID: 0034610468     PISSN: 00097322     EISSN: None     Source Type: Journal    
DOI: 10.1161/01.CIR.102.23.2861     Document Type: Article

References (29)

1. The emerging concept of vascular remodeling
2. Smooth muscle cell migration and matrix metalloproteinase expression after arterial injury in the rat
3. Immunolocalization of matrix metalloproteinases in rabbit carotid arteries after balloon denudation
4. Role of matrix metalloproteinases and their tissue inhibitors in the regulation of coronary cell migration
5. Mouse model of arterial injury
6. Urokinase but not tissue plasminogen activator mediates arterial neointima formation in mice
7. Remodeling with neointima formation in the mouse carotid artery after cessation of blood flow
8. Cytokine-stimulated human vascular smooth muscle cells synthesize a complement of enzymes required for extracellular matrix digestion
9. Ki-ras activation in vitro affects G1 and G2 M cell-cycle transit times and apoptosis
10. Involvement of extracellular-matrix-degrading metalloproteinases in rabbit aortic smooth-muscle cell proliferation
11. A possible role for MMP-2 and MMP-9 in the migration of primate arterial smooth muscle cells through native matrix
12. Function of the plasminogen/plasmin and matrix metalloproteinase systems after vascular injury in mice with targeted inactivation of fibrinolytic system genes
13. Flow regulation of 72-kD collagenase IV (MMP-2) after experimental arterial injury
14. Vascular remodeling in response to altered blood flow is mediated by fibroblast growth factor-2
15. Remodeling and neointimal formation in the carotid artery of normal and P-selectin-deficient mice
16. Vascular injury causes neointimal formation in angiotensin II type 1a receptor knockout mice
17. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques
18. Comparison of cleavage site specificity of gelatinases A and B using collagenous peptides
19. Wound healing: A paradigm for lumen narrowing after arterial reconstruction
20. Arterial remodeling after coronary angioplasty: A serial intravascular ultrasound study
21. Remodeling rather than neointimal formation explains luminal narrowing after deep vessel wall injury: Insights from a porcine coronary (re)stenosis model
22. Expression of nonmuscle myosin heavy chain-B isoform in the vessel wall of porcine coronary arteries after balloon angioplasty
23. Vascular myofibroblasts: Lessons from coronary repair and remodeling
24. Contribution of adventitial myofibroblasts to vascular remodeling and lesion formation after experimental angioplasty in pig coronary arteries
25. Origin of extracellular matrix synthesis during coronary repair
26. Human 92- and 72-kilodalton type IV collagenases are elastases
27. Gelatinase B: Structure, regulation, and function
28. Synthetic inhibitors of matrix metalloproteinases
29. Divergent effects of tissue inhibitor of metalloproteinase-1, -2, or -3 overexpression on rat vascular smooth muscle cell invasion, proliferation, and death in vitro: TIMP-3 promotes apoptosis