Copper-induced inflammatory reactions of rat carotid arteries mimic restenosis/arteriosclerosis-like neointima formation

Völker, Wolfgang; Dorszewski, Anja; Unruh, V.; Robenek, Horst; Breithardt, Günter; Buddecke, Eckhart

doi:10.1016/s0021-9150(96)06039-x

Cited by 48 publications

(37 citation statements)

References 18 publications

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“…Their number was inversely correlated with the levels of type VIII collagen. In contrast to other studies that suggested combined injury and hypercholesterolemia 46,47 or inflammation 48 as stimulators of the infiltration of monocytes and macrophages into the adventitia, our data give evidence that deposition of lipids in the adventitia might directly attract inflammatory cells. However, indirect mechanisms, such as lipid-induced ECM remodeling, might facilitate adventitial infiltration by inflammatory cells as well.…”

Section: Discussioncontrasting

confidence: 99%

Cholesterol-Induced Changes of Type VIII Collagen Expression and Distribution in Carotid Arteries of Rabbit

Plenz

Dorszewski²,

Völker³

et al. 1999

ATVB

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Abstract-Lipoproteins play a major role in cardiovascular disease and atherosclerosis. In the vascular wall, they strongly influence the organization of extracellular matrix. The present study set out to investigate the changes in the extracellular matrix of the vessel wall induced by atherogenic diet, focusing on type VIII collagen, a vascular collagen that has not previously been investigated in detail. The influence of cholesterol diet on the expression, distribution, and deposition of type VIII collagen was examined in carotid arteries of New Zealand White rabbits. Carotid arteries of rabbits receiving diet supplemented with 1% cholesterol for 6 weeks and those on the same regimen followed by normal chow for 1 day, 10 days, 5 weeks, and 12 weeks were studied and compared with controls not exposed to the cholesterol diet. Carotid arteries of normocholesterolemic rabbits contained type VIII collagen-expressing cells in all layers, with focal accumulations of expressing cells in the subendothelial areas, the outer medial zone, and the adventitia. In response to cholesterol diet, type VIII collagen synthesis was reduced in media and adventitia and the distribution patterns changed. Expressing cells were found predominantly in the endothelium, and type VIII collagen accumulated in the intimal space.Immunogold labeling for electron microscopy revealed that type VIII collagen in the intima is associated with microfibrils extending from the internal elastic lamina. Withdrawal of cholesterol resulted in reestablishment of the normal distribution pattern. Northern and Western blot analyses supported the immunoconfocal and in situ hybridization data, demonstrating decreased type VIII collagen expression in response to cholesterol diet and progressive recovery to normal levels with time after withdrawal of cholesterol.

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Section: Discussioncontrasting

confidence: 99%

Cholesterol-Induced Changes of Type VIII Collagen Expression and Distribution in Carotid Arteries of Rabbit

Plenz

Dorszewski²,

Völker³

et al. 1999

ATVB

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“…The construction was a major modification of a similar cuff used in rats. 32 The two-part silicone product was combined with the copper dust and then degassed under vacuum. Stainless steel molds, which mimic the size of the diameter of a mouse carotid artery, were used in the construction.…”

Section: Copper/silicone Cuff Constructionmentioning

confidence: 99%

Remodeling of the Vessel Wall after Copper-Induced Injury Is Highly Attenuated in Mice with a Total Deficiency of Plasminogen Activator Inhibitor-1

Ploplis

Cornelissen

Sandoval-Cooper

et al. 2001

The American Journal of Pathology

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Clinical studies have indicated that high plasma levels of fibrinogen, or decreased fibrinolytic potential, are conducive to an increased risk of cardiovascular disease. Other investigations have shown that insoluble fibrin promotes atherosclerotic lesion formation by affecting smooth muscle cell proliferation, collagen deposition, and cholesterol accumulation. To directly assess the physiological impact of an imbalanced fibrinolytic system on both early and late stages of this disease, mice deficient for plasminogen activator inhibitor-1 (PAI-1 ؊/؊ ) were used in a model of vascular injury/repair, and the resulting phenotype compared to that of wild-type (WT) mice. A copper-induced arterial injury was found to generate a lesion with characteristics similar to many of the clinical features of atherosclerosis. Fibrin deposition in the injured arterial wall at early (7 days) and late (21 days) times after copper cuff placement was prevalent in WT mice, but was greatly diminished in PAI-1 ؊/؊ mice. A multilayered neointima with enhanced collagen deposition was evident at day 21 in WT mice. In contrast, only diffuse fibrin was identified in the adventitial compartments of arteries from PAI-1 ؊/؊ mice, with no evidence of a neointima. Neovascularization was observed in the adventitia and was more extensive in WT arteries, relative to PAI-1 ؊/؊ arteries. Additionally, enhanced PAI-1 expression and fat deposition were seen only in the arterial walls of WT mice. The results of this study emphasize the involvement of the fibrinolytic system in vascular repair processes after injury and indicate that alterations in the fibrinolytic balance in the vessel wall have a profound effect on the development and progression of vascular lesion formation. Among the critical proteins that constitute the fibrinolytic system in mammals are the zymogen, plasminogen, and its activated product, plasmin, a serine protease; plasminogen activators, eg, urokinase-type plasminogen activator (uPA) and tissue-type plasminogen activator, which are also serine proteases; receptors for these proteins, eg, the uPA receptor (uPAR); serpin-type inhibitors, eg, plasminogen activator inhibitor-1 (PAI-1); and fibrinogen/fibrin. In addition to the clot-dissolving capacity of this system, a number of in vitro and in vivo studies have implicated plasmin as playing an important role in proteolytic processes associated with cell migration, which is a pivotal event in the inflammatory response. These effects have been attributed to the ability of components of the fibrinolytic system to assemble on cell surfaces through interaction with specific receptors, such as ␣-enolase for plasminogen

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“…Accumulating evidence suggest that copper plays a fundamental role in regulating cell growth involved in physiological repair processes such as wound healing and angiogenesis as well as in various pathophysiologies including tumor growth, atherosclerosis, and neuron degenerative diseases (1)(2)(3)(4)(5)(6)(7)(8)(9)(10)(11)(12). Of note, hyperproliferative lesions in cancer and atherosclerosis have higher copper levels in cell nuclei than normal tissues (13)(14)(15), while copper chelation prevents tumor growth and neointimal thickening after vascular injury (9 -12).…”

mentioning

confidence: 99%

Novel Role of Antioxidant-1 (Atox1) as a Copper-dependent Transcription Factor Involved in Cell Proliferation

Itoh

Kim

Nakagawa

et al. 2008

Journal of Biological Chemistry

253

234

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Copper-induced inflammatory reactions of rat carotid arteries mimic restenosis/arteriosclerosis-like neointima formation

Cited by 48 publications

References 18 publications

Cholesterol-Induced Changes of Type VIII Collagen Expression and Distribution in Carotid Arteries of Rabbit

Cholesterol-Induced Changes of Type VIII Collagen Expression and Distribution in Carotid Arteries of Rabbit

Remodeling of the Vessel Wall after Copper-Induced Injury Is Highly Attenuated in Mice with a Total Deficiency of Plasminogen Activator Inhibitor-1

Novel Role of Antioxidant-1 (Atox1) as a Copper-dependent Transcription Factor Involved in Cell Proliferation

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