Stromelysin-1 (Matrix Metalloproteinase-3) and Tissue Inhibitor of Metalloproteinase-3 Are Overexpressed in the Wall of Abdominal Aortic Aneurysms

Carrell, Tom; Burnand, K. G.; Wells, Graham; Clements, John M.; Smith, Alberto

doi:10.1161/hc0402.102621

Cited by 132 publications

(101 citation statements)

References 36 publications

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“…The observed differences could not be attributed to a particular cardiovascular risk factor because the presence of dyslipidemia, arterial hypertension, diabetes and smoking, were similar between both groups. There are conflicting reports on the expression of MMPs in relation to aneurysms [7][8][9][10], but in general, the majority of the studies have reported the involvement of at least MMP-2 and MMP-9 in abdominal aortic aneurysms [24]. A novel finding of our study was an increased expression of MMP-1 and-3, but not MMP-9 in femoral aneurysms, suggesting that regional differences in the proteolytic mechanisms may be operating in different arterial beds.…”

Section: Discussionmentioning

confidence: 48%

“…MMP-1 has been related to cardiac hypertrophy, dilation and systolic dysfunction in the hearts of transgenic mice [25]. On the other hand, MMP-3 would contribute to plaque destabilization by degrading ECM components, and could also promote aneurysm formation by degrading the elastic lamina [9]. These effects may be directly mediated by MMP-3 or by activation of other proMMPs [7].…”

Section: Discussionmentioning

confidence: 99%

“…Excessive or inappropriate expression of MMPs is known to contribute to the pathogenesis of cardiovascular diseases (atherosclerosis plaque rupture and aneurysm formation). There is evidence of increased expression of some MMPs, particularly gelatinases and/or stromelysin-1, in abdominal aortic aneurysms [7][8][9][10]. MMP activity is controlled by specific inhibitors (TIMPs); four members of the tissue inhibitor family have been identified: TIMP-1, -2, -3, and -4 [11,12].…”

Section: Introductionmentioning

confidence: 99%

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Different expression of MMPs/TIMP-1 in human atherosclerotic lesions. Relation to plaque features and vascular bed

et al. 2003

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Background: Proteolytic imbalance might determine arterial remodeling and plaque destabilization in atherosclerotic vessels. The aim of this study was to examine differences in the patterns of metalloproteinases (MMPs) and MMP inhibitor (TIMP-1) expression in advanced human atheromas, both in relation to the plaque features and the vascular bed involved. Methods and results: Immunohistochemistry for MMP-1, -3, -9 and TIMP-1 as well as the collagen content were measured in vascular sections from patients undergoing peripheral revascularization (carotid n = 11, femoral n = 23) and aorto-coronary bypass surgery (mammary arteries n = 20, as controls). Increased expression of all MMPs was detected in atherosclerotic as compared with control sections (P<0.01). Aneurismal plaques showed a significant increase of MMP-1 and-3 and a reduction in total collagen (P<0.05) in relation to occlusive lesions. Calcification areas in atherosclerotic plaques were consistently associated with increased TIMP-1 expression (P<0.01). Finally, MMP-9 expression was higher in occlusive lesions from carotid than femoral arteries (P<0.01). Conclusions: Aneurysm lesions expressed higher MMP-1 and-3 expression than occlusive plaques, and MMP-9 was mainly detected in carotid as compared with femoral arteries. TIMP-1 was associated with arterial calcification. These differences in the MMPs/TIMP-1 expression might determine the evolution of advanced atherosclerotic plaques and contribute to its vulnerability.

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Section: Discussionmentioning

confidence: 48%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Different expression of MMPs/TIMP-1 in human atherosclerotic lesions. Relation to plaque features and vascular bed

et al. 2003

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“…1 Increased MMP-9 levels were detected in plasma of AAA patients and patients with acute coronary syndromes. 2,3 In addition, aneurysm and atherosclerotic tissues overexpress MMP-1, -2, -3, -7, -8, -9, -12, -13, -14, and -17 (Carrell et al 4 and references therein).…”

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confidence: 99%

Loss of Matrix Metalloproteinase-9 or Matrix Metalloproteinase-12 Protects Apolipoprotein E–Deficient Mice Against Atherosclerotic Media Destruction but Differentially Affects Plaque Growth

et al. 2004

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Background-Epidemiological and histological evidence implicates proteinases of the matrix metalloproteinase (MMP) family in atherosclerosis and aneurysm formation. We previously indicated a role for urokinase-type plasminogen activator in atherosclerotic media destruction by proteolytic activation of MMPs. However, the role of specific MMPs, such as MMP-9 and MMP-12, in atherosclerosis remains undefined. Methods and Results-MMP-9 -or MMP-12-deficient mice were crossed in the atherosclerosis-prone apolipoprotein E-deficient background and fed a cholesterol-rich diet. Mice were killed at 15 or 25 weeks of diet to study intermediate and advanced lesions, respectively. Loss of MMP-9 reduced atherosclerotic burden throughout the aorta and impaired macrophage infiltration and collagen deposition, while MMP-12 deficiency did not affect lesion growth. MMP-9 or MMP-12 deficiency conferred significant protection against transmedial elastin degradation and ectasia in the atherosclerotic media. Conclusions-This study is the first to provide direct genetic evidence for a significant involvement of MMP-9, but not of MMP-12, in atherosclerotic plaque growth. In addition, deficiency of MMP-9 or MMP-12 protected apolipoprotein E-deficient mice against atherosclerotic media destruction and ectasia, mechanisms that implicate the involvement of

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“…Among these, an important role was attributed to MMPs [1,2,19,23,24] that determine, in response to biochemical and local hemodynamic insults, abnormal extracellular matrix degradation promoting an exuberant expansive remodeling of the vascular wall and thus the development of CAE [25].…”

Section: Discussion:-mentioning

confidence: 99%

Matrix Metalloproteinases and Coronary Artery Ectasia.

Levantino¹,

Raspanti²,

Evola³

et al. 2017

IJAR

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Background: Coronary artery ectasia is the abnormal dilatation of one or more coronary segments. Although the pathogenetic mechanisms underlying CAE are largely unknown, it seems that some of the extracellular matrix degrading enzymes such as matrix metalloproteinases (mmps) can play an important role in the development of this condition. The aim of our study was to evaluate the relationship between MMP-9 and the development of CAE as well as the role played by the inflammatory process in this condition. Materials And Methods: In our retrospective study we have enrolled a series of 79 patients: 47 presented, on coronary angiography, focal or diffuse ectasia of coronary arteries (cases), 32 had a free coronary tree or without hemodynamically significant stenosis (controls). All patients were subjected to blood sampling for the dosage of MMP-9 and Creactive protein (CRP). Results: In our study we found that the most involved coronary artery in CAE was the right coronary artery. Serum levels of MMP-9 were higher in the patients with CAE (5.011 mcg / ml vs. 3.93 mcg / ml, p = 0,07) although not statistically significant, in direct proportion to the number of involved vessels (p = 0.025). Serum CRP levels were higher in patients with CAE (5.12 mg / dl vs. 2.18 mg / dl, p = 0.4) although not statistically significant, in direct proportion to the number of involved vessels (p = 0.001). Conclusions: We found a possible relationship between elevated levels of MMP-9 and CAE, as well as the relationship between levels of MMP-9 and severity of the CAE. Furthermore we found a possible relationship between elevated CRP levels and CAE and there was a directly proportional relationship between the increase of CRP and extension of the CAE.

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Stromelysin-1 (Matrix Metalloproteinase-3) and Tissue Inhibitor of Metalloproteinase-3 Are Overexpressed in the Wall of Abdominal Aortic Aneurysms

Cited by 132 publications

References 36 publications

Different expression of MMPs/TIMP-1 in human atherosclerotic lesions. Relation to plaque features and vascular bed

Different expression of MMPs/TIMP-1 in human atherosclerotic lesions. Relation to plaque features and vascular bed

Loss of Matrix Metalloproteinase-9 or Matrix Metalloproteinase-12 Protects Apolipoprotein E–Deficient Mice Against Atherosclerotic Media Destruction but Differentially Affects Plaque Growth

Matrix Metalloproteinases and Coronary Artery Ectasia.

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