Clinica Chimica Acta

1991

DOI: 10.1016/0009-8981(91)90084-p

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Human aortic elastin from normal individuals and atherosclerotic patients: lipid and cation contents; susceptibility to elastolysis

Joëlle Saulnier

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Cited by 26 publications

(18 citation statements)

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“…4 On the other hand, increased elastolytic activity is associated with severity of atherosclerosis in the aorta. 20 We found elastin in the subendothelial space and in the ruptured areas in the plaques associated with symptoms. Shoulders of these plaques had stronger elastin staining, possibly related to the turbulence and strong hemodynamic forces that these regions have to attenuate.…”

Section: Discussionmentioning

confidence: 95%

Changes Related to Age and Cerebrovascular Symptoms in the Extracellular Matrix of Human Carotid Plaques

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Background and Purpose-Many processes involved in the pathogenesis of atherosclerosis result in modifications of the extracellular matrix. These changes not only determine the mechanical stability of atherosclerotic lesions but can directly or indirectly influence further development of the lesions. The purpose of the present study was to compare the matrix composition of human carotid plaques from symptomatic patients with those obtained from patients without symptoms. Furthermore, matrix changes related to age were studied. Methods-Thirty atherosclerotic carotid plaques were removed by endarterectomy from 27 patients and divided into 2 groups on the basis of the presence of ipsilateral symptoms. The plaques were homogenized, and the total levels of the major components of the extracellular matrix were determined. Results-Plaques associated with symptoms were characterized by increased levels of elastin (1.58Ϯ0.46 versus 1.24Ϯ0.40 mg/g wet wt; Pϭ0.03) and decreased levels of hydroxyapatite (45.1Ϯ46.3 versus 131.4Ϯ111.7 mg/g wet wt; Pϭ0.02) compared with asymptomatic plaques. The increase in elastin in plaques from symptomatic patients was due to elevated levels of an intermediate-size fraction, as determined by liquid chromatography. Collagen and sulfated glycosaminoglycans were present in equal amounts in both groups. Elastin content in carotid plaques decreased with age. Conclusions-Carotid plaques from symptomatic patients have lower levels of hydroxyapatite than those from asymptomatic patients. The present study also raises the possibility that non-cross-linked forms of elastin, increased in plaques associated with symptoms, could be a marker of plaque vulnerability and/or directly induce harmful cellular activities or increase lipoprotein retention in the vascular wall.

“…4 On the other hand, increased elastolytic activity is associated with severity of atherosclerosis in the aorta. 20 We found elastin in the subendothelial space and in the ruptured areas in the plaques associated with symptoms. Shoulders of these plaques had stronger elastin staining, possibly related to the turbulence and strong hemodynamic forces that these regions have to attenuate.…”

Section: Discussionmentioning

confidence: 95%

Changes Related to Age and Cerebrovascular Symptoms in the Extracellular Matrix of Human Carotid Plaques

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,

²

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et al. 2003

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Background and Purpose-Many processes involved in the pathogenesis of atherosclerosis result in modifications of the extracellular matrix. These changes not only determine the mechanical stability of atherosclerotic lesions but can directly or indirectly influence further development of the lesions. The purpose of the present study was to compare the matrix composition of human carotid plaques from symptomatic patients with those obtained from patients without symptoms. Furthermore, matrix changes related to age were studied. Methods-Thirty atherosclerotic carotid plaques were removed by endarterectomy from 27 patients and divided into 2 groups on the basis of the presence of ipsilateral symptoms. The plaques were homogenized, and the total levels of the major components of the extracellular matrix were determined. Results-Plaques associated with symptoms were characterized by increased levels of elastin (1.58Ϯ0.46 versus 1.24Ϯ0.40 mg/g wet wt; Pϭ0.03) and decreased levels of hydroxyapatite (45.1Ϯ46.3 versus 131.4Ϯ111.7 mg/g wet wt; Pϭ0.02) compared with asymptomatic plaques. The increase in elastin in plaques from symptomatic patients was due to elevated levels of an intermediate-size fraction, as determined by liquid chromatography. Collagen and sulfated glycosaminoglycans were present in equal amounts in both groups. Elastin content in carotid plaques decreased with age. Conclusions-Carotid plaques from symptomatic patients have lower levels of hydroxyapatite than those from asymptomatic patients. The present study also raises the possibility that non-cross-linked forms of elastin, increased in plaques associated with symptoms, could be a marker of plaque vulnerability and/or directly induce harmful cellular activities or increase lipoprotein retention in the vascular wall.

“…8,10 These studies also show that MMP-2 inhibition or cathepsin S ablation in the context of uremia abrogates the development of arterial medial calcification. 8,9 Interestingly, calcified aortic elastin is more susceptible to proteolysis than uncalcified elastin, 29 raising the possibility of a vicious cycle in which elastin fragmentation leads to mineralization, which, in turn, promotes further degradation. Unfortunately, we do not have imaging data to directly examine the relationship between elastin degradation markers and aortic calcification burden in our patients, and future work should certainly address this point.…”

Section: Discussionmentioning

confidence: 99%

Elastin Degradation Is Associated With Progressive Aortic Stiffening and All-Cause Mortality in Predialysis Chronic Kidney Disease

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et al. 2012

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Abstract-In the large conduit arteries, elastin is important in maintaining vascular compliance. Studies in animal models suggest that elastin degradation may promote arteriosclerotic vascular changes. There is already a well-established link between aortic stiffening and mortality in the general population and in patients undergoing dialysis. Elastin degradation is mediated by several proteases, including matrix metalloproteinase 2 and cathepsin S. Elastin turnover may be inferred by measuring serum levels of elastin-derived peptides. We analyzed the serum concentration of these biomarkers, their endogenous inhibitors, and aortic pulse wave velocity in 200 patients with stages 3 and 4 chronic kidney disease and then serially in a subgroup of 65 patients over 36 months. Serum matrix metalloproteinase 2, cathepsin S, and elastin-derived peptide levels were independently associated with baseline aortic pulse wave velocity and changes in stiffness over the follow-up period. Higher matrix metalloproteinase 2 and elastin-derived peptide levels were also independently associated with preexisting cardiovascular disease. In multivariable Cox regression, higher serum elastin-derived peptide levels were independently associated with increased all-cause mortality (hazard ratio per SD increaseϭ1.78; Pϭ0.021). In predialysis chronic kidney disease, elastin degradation is an important determinant of arterial stiffness and is associated with all-cause mortality. 1 Loss of elastin leads to an increase in the collagen:elastin ratio and augmented mechanical loading of stiffer collagen fibers. With age, vascular smooth muscle cells (VSMCs) become less contractile, and there are increased rates of cellular senescence and death.2 Together, these changes contribute to the loss of intrinsic elasticity and progressive stiffening of the arterial wall.3 In addition to promoting arteriosclerosis, elastin degradation also stimulates intimal VSMC invasion, neointima formation, and plaque destabilization and, thus, may also be an important factor in the pathogenesis of atherosclerotic disease. Age-associated arterial remodeling is accelerated in patients with chronic kidney disease (CKD), who have a vastly elevated cardiovascular risk compared with the general population. 5 Although not a universal finding, arterial stiffness, as measured by various methods, has been associated with decline in renal function in patients with CKD 6-8 and is a strong predictor of cardiovascular risk and all-cause mortality in patients with end-stage renal failure 9 and in non-CKD populations. 10Extracellular matrix turnover is mediated by a number of elastolytic proteinases, including Zn 2ϩ /Ca 2ϩ -dependent matrix metalloproteinases (MMPs; eg, MMP-2) and cathepsin cysteine proteases, such as cathepsin S. These proteases are mainly secreted by activated macrophage, resident myofibroblasts, or VSMCs but are also expressed intracellularly in a wide range of cell types. 4 The activities of MMP-2 and cathepsin S are partly regulated by the concentration of endog...

“…40,41) ET-1 is known as an activator of atherosclerosis. Therefore, the results of this paper suggest that inhibition of tropoelastin and LO mRNA expression by ET-1 may cause inhibition of the elastin cross-linking processes in the aorta and result in a destabilization of the aortic wall such as occurs in the disease of atherosclerosis.…”

Section: Discussionmentioning

confidence: 99%

Endothelin-1 Down-Regulates Expression of Tropoelastin and Lysyl Oxidase mRNA in Cultured Chick Aortic Smooth Muscle Cells.

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JOURNAL OF HEALTH SCIENCE

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Endothelin-1 (ET-1) is known as a potent stimulator of cell proliferation and as a vasoconstrictor. It is believed that ET-1 contributes to the development of arterial diseases such as atherosclerosis. In this study, we demonstrated the expression of tropoelastin and lysyl oxidase (LO) on gene levels as induced by ET-1 in cultured smooth muscle cells (SMCs). ET-1 stimulated cell proliferation in a dose-dependent manner, and the level of this proliferation increased about 1.3-fold at 100 nM of ET-1. ET-1 suppressed the tropoelastin protein synthesis in a dose-dependent and time-dependent manner. In addition, ET-1 dose-dependently suppressed the tropoelastin and LO mRNA expression. The tropoelastin and LO mRNA levels decreased to about half and 4/5, respectively, at 100 nM of ET-1. The inhibition of elastin synthesis was completely prevented by BQ123, an endothelin receptor A (ET A ) antagonist. These results indicate that ET-1 can modulate the tropoelastin and LO mRNA expression via an ET A receptor in cultured SMC and that the regulator for elastin expression may play an important role in elastogenesis and SMC proliferation during the development of atherosclerosis.

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