Collagen and elastin degradation by matrix metalloproteinases and tissue inhibitors of matrix metalloproteinase in aortic dissection

Ishii, Toshiharu; Asuwa, Noriko

doi:10.1053/hupa.2000.7642

Cited by 113 publications

(97 citation statements)

References 19 publications

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“…Primary coronary artery dissections, as in our case, are much less common than secondary dissections, and their etiology remains unclear. Associations of primary coronary artery dissections with female sex, exercise, pregnancy and postpartum state, coronary artery disease, connective tissue disorders and hemorrhage into the vasovasorum and periadventitial inflammation, have been noted [1][2][3][4][5][6][7]. Our case confirmed association of primary coronary artery dissections with female sex.…”

Section: Discussionsupporting

confidence: 78%

“…The cause of spontaneous coronary dissection is poorly understood. There are reported associations with female sex, exercise, pregnancy and postpartum state, coronary artery disease, connective tissue disorders and hemorrhage into the vasovasorum and periadventitial inflammation [1][2][3][4][5][6][7]. Most cases have no identifiable risk factor [1,7].…”

Section: Introductionmentioning

confidence: 99%

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Spontaneous Coronary Dissection with Dissection of Ascending Aorta and Cardiac Tamponade

Stojanović¹,

Ilić²,

Stojanović³

et al. 2014

J Vasc Med Surg

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Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Spontaneous Coronary Dissection with Dissection of Ascending Aorta and Cardiac Tamponade

Stojanović¹,

Ilić²,

Stojanović³

et al. 2014

J Vasc Med Surg

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“…More specifically, the MMPs MMP-2 and MMP-9 are thought to favor the pathogenesis, whereas the specific inhibitor TIMP-1 is thought to be preventive. 1,4,38,39 The results of the oligonucleotide array suggested a possible increase in mRNA levels of TIMP-1, whereas there were no apparent differences in MMP levels. These results were confirmed by real-time PCR: NOX1 deficiency had no effect on MMP-2 and MMP-9 mRNA levels ( Figure 3D and 3E).…”

Section: Nox1 and Mmpsmentioning

confidence: 95%

NOX1 Deficiency Protects From Aortic Dissection in Response to Angiotensin II

et al. 2007

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Abstract-Oxidative stress leads to vascular damage and participates in the pathomechanisms of aortic dissection and aneurysm formation. Here we study aortic dissection in mice deficient in the superoxide-generating reduced nicotinamide-adenine dinucleotide phosphate oxidase NOX1. Seven days of treatment with the hypertensive agent angiotensin II (3 mg/kg per day) led to aortic dissection in 23% of wild-type C57BL/6J mice but in only 4% of NOX1-deficient mice (Pϭ0.05). In contrast, treatment of wild-type C57BL/6J mice with the hypertensive agent norepinephrine (12 mg/kg per day), did not lead to aortic dissection or sudden death, suggesting that hypertension is not sufficient to cause aortic dissection. Interestingly, norepinephrine-dependent blood pressure elevations were conserved in NOX1-deficient mice, demonstrating that, different from angiotensin II, it acts through NOX1-independent hypertensive mechanisms. The resistance of NOX1-deficient mice to angiotensin II-induced aortic dissection suggests a role for NOX1-dependent alterations of the vascular wall. We, therefore, studied gene expression and protease/inhibitor equilibrium. cDNA array analysis demonstrated differential effects of angiotensin II on gene expression in wild-type and NOX1-deficient mice. Tissue inhibitor of metalloproteinase 1 was increased both on the mRNA and the protein level in aortas from NOX1-deficient mice. Thus, our results demonstrate that NOX1 is involved in the mechanisms of angiotensin II-dependent aortic dissection. As one underlying mechanism, we have identified NOX1-dependent suppression of tissue inhibitor of metalloproteinase 1 expression, which could lead to tissue damage through an altered protease/inhibitor balance. Key Words: NOX1 Ⅲ nicotinamide-adenine dinucleotide phosphate oxidase Ⅲ blood pressure Ⅲ aortic dissection Ⅲ angiotensin II A ortic dissections and formation of aneurysms are serious and frequent medical conditions that are the consequence of damage to the vascular wall. Animals model play a key role in understanding their pathomechanisms. 1 Angiotensin II perfusion in mice has become a particularly valuable model for this pathological process. 2-5 Angiotensin II-induced vascular alterations include the following: (1) sustained blood pressure elevations; (2) increase in the thickness of the aortic media through mechanisms including smooth muscle hyperplasia, smooth muscle proliferation, and accumulation of extracellular matrix (ECM) proteins; (3) markers of inflammation, including oxidative damage to the vascular tissue, infiltration of monocytes/macrophages, and activation of matrix metalloproteinases; and (4) formation of aortic dissection and aneurysms. 1,4 Angiotensin II-dependent signal transduction is complex and involves Ն2 different receptors and the activation of multiple intracellular signaling pathways. 6,7 There is now increasing evidence that reactive oxygen species (ROS) are an important part of angiotensin II-dependent signal transduction 8 -12 involved in the pathogenesis of aortic aneurysms...

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“…Elastin is readily degraded by the serine proteases pancreatic and neutrophil (or leukocyte) elastase, as well as several matrix metalloproteinases including MMP-2, MMP-7 (matrilysin), MMP-9 and MMP-12 (metalloelastase) [24,29,39]. In the disc, only limited descriptions of the presence and function of these enzymes currently exist.…”

Section: Roles Of Elastic Fibres In the Ageing And Degeneration Of Thmentioning

confidence: 99%

The elastic fibre network of the human lumbar anulus fibrosus: architecture, mechanical function and potential role in the progression of intervertebral disc degeneration

Smith

Fazzalari

2009

Eur Spine J

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Elastic fibres are critical constituents of dynamic biological structures that functionally require elasticity and resilience. The network of elastic fibres in the anulus fibrosus of the intervertebral disc is extensive, however until recently, the majority of histological, biochemical and biomechanical studies have focussed on the roles of other extracellular matrix constituents such as collagens and proteoglycans. The resulting lack of detailed descriptions of elastic fibre network architecture and mechanical function has limited understanding of the potentially important contribution made by elastic fibres to healthy disc function and their possible roles in the progression of disc degeneration. In addition, it has made it difficult to postulate what the consequences of elastic fibre related disorders would be for intervertebral disc behaviour, and to develop treatments accordingly. In this paper, we review recent and historical studies which have examined both the structure and the function of the human lumbar anulus fibrosus elastic fibre network, provide a synergistic discussion in an attempt to clarify its potentially critical contribution both to normal intervertebral disc behaviour and the processes relating to its degeneration, and recommend critical areas for future research.

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Collagen and elastin degradation by matrix metalloproteinases and tissue inhibitors of matrix metalloproteinase in aortic dissection

Cited by 113 publications

References 19 publications

Spontaneous Coronary Dissection with Dissection of Ascending Aorta and Cardiac Tamponade

Spontaneous Coronary Dissection with Dissection of Ascending Aorta and Cardiac Tamponade

NOX1 Deficiency Protects From Aortic Dissection in Response to Angiotensin II

The elastic fibre network of the human lumbar anulus fibrosus: architecture, mechanical function and potential role in the progression of intervertebral disc degeneration

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