Calcium and Elastin in Human Arteriosclerosis

Lansing, Albert I.; Alex, Morris; Rosenthal, Theodore

doi:10.1093/geronj/5.2.112

Cited by 91 publications

(34 citation statements)

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“…Furthermore, over the age range of 81-103 yr, the aortic wall elastin content fell, and the calcium content rose concomitantly (63). Likewise, in coronary arteries, calcification was accompanied by elastic fiber fragmentation (63). These observations suggest that medial calcification involves destruction of elastin (5).…”

Section: Calcification Of Medial Elastic Fibers: Elastocalcinosismentioning

confidence: 92%

“…The Blumenthal group also showed that, in any given age group, the calcium and phosphorus contents of aortic elastic tissue were always substantially higher than those of the whole aorta (128). Furthermore, over the age range of 81-103 yr, the aortic wall elastin content fell, and the calcium content rose concomitantly (63). Likewise, in coronary arteries, calcification was accompanied by elastic fiber fragmentation (63).…”

Section: Calcification Of Medial Elastic Fibers: Elastocalcinosismentioning

confidence: 97%

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Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences

Atkinson¹

2008

Journal of Applied Physiology

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Atkinson J. Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences. J Appl Physiol 105: 1643-1651, 2008. First published September 4, 2008 doi:10.1152/japplphysiol.90476.2008.-With age, the calcium content of the arterial wall increases. Calcification occurs at two main levels: intimal plaques and the medial elastic fiber network. The latter has been referred to as medial elastocalcinosis and is the subject of this review. The mechanisms involved in elastocalcinosis are complex and involve polar, apolar, and active processes. Vascular calcification may be species specific to humans. As laboratory animals, such as the rat, grow old, they suffer from only very mild arterial calcification. Different animal models of induction of massive arterial calcification by pharmacological and other means exist. Although extrapolation from such models to the clinical situation in terms of etiology is difficult, such models could be useful in the nonclinical study of the pathophysiological consequences of vascular calcification. Vascular calcification modifies arterial wall stiffness, and this could have clinically significant consequences on cardiac function and downstream circulatory control.artery; calcium; wall stiffness; aging Development of the Concept of ElastocalcinosisSeveral recent reviews deal with the subject of elastocalcinosis (1,21,25,41,54,56,82,108).Age-linked vascular calcification has been known since the nineteenth century (85,122). It appears to be "specific" in that vascular wall calcium and phosphorus contents increase with age, whereas there are no significant increases in the aortic content of most other elements, such as sodium, potassium, and magnesium (128). Vascular calcification linked to age is also specific for arteries and does not involve other soft tissues, such as veins (57,60,117). Vascular calcification is associated with hypertension. Blumenthal et al. (9) showed that the onset of arterial calcification occurs at an earlier age in hypertensive subjects. The association in humans between arterial calcification and hypertension has since been reported by many investigators (75). The etiology of the complex multifactorial interactions, however, between hypertension (and associated changes in vascular wall mechanics) and amplification of calcification remains obscure.Vascular calcification can occur in localized intimal plaques and in a diffuse fashion in the media (53), and often there is no indication in published reports of where samples were taken. Méndez and Tejada (76) reported that the calcium content of plaques is 10-fold higher than that of "plaque-free" artery. Thus "contamination" of samples with plaque material could mask medial, diffuse elastocalcinosis. It is to be noted that the calcium content of "normal" intima (i.e., free of plaques and fatty streaks) is low and shows only a slight increase with age (6, 29). Medial elastocalcinosis independent of atheroma-associated calcification has been demonstrated by Elliot and McGra...

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Section: Calcification Of Medial Elastic Fibers: Elastocalcinosismentioning

confidence: 92%

Section: Calcification Of Medial Elastic Fibers: Elastocalcinosismentioning

confidence: 97%

Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences

Atkinson¹

2008

Journal of Applied Physiology

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“…The plaque areas and adjacent normal intimae were pooled separately for each aorta and then minced and homogenized. Elastin was prepared from each set of tissue homogenates by boiling with 0.1 N NaOH according to a modification of the method of Lansing, Rosenthal, Alex, and Dempsey (13) (14)(15)(16). The blood was collected in 50-ml Lusteroid tubes and allowed to clot at 260C for approximately 1 h. Serum was separated by centrifugation at 2400 rpm for 30 min at 4°C.…”

Section: Methods Elastin Preparationmentioning

confidence: 99%

The Interaction of Serum and Arterial Lipoproteins with Elastin of the Arterial Intima and Its Role in the Lipid Accumulation in Atherosclerotic Plaques

Kramsch¹,

Hollander²

1973

J. Clin. Invest.

127

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A B S T R A C T Arterial elastin appears to be a proteinlipid complex with the lipid component being bound to elastin peptide groups. In atherosclerotic lesions the lipid content of elastin increases progressively with increasing severity of atherosclerosis. The increases in the lipid content of plaque elastin are mainly due to large increases in cholesterol with about 80% of the cholesterol being cholesterol ester. This deposition of cholesterol in elastin accounts for a substantial part of the total cholesterol accumulation in atherosclerotic lesions of all stages. The present in vitro study suggests that the mechanism involved in the deposition of lipids in arterial elastin may be an interaction of the elastin protein with serum or arterial low density or very low density lipoproteins (LDL and VLDL) resulting in a transfer of lipids, but not of lipoprotein protein to the elastin. No significant lipid transfer occurred from the high density lipoproteins or chylomicrons. The amount of lipid taken up by plaque elastin was strikingly higher than by normal elastin and consisted mainly of cholesterol with over 80% of the cholesterol being cholesterol ester. The precondition for the lipid accumulation in plaque elastin appeared to be an altered amino acid composition of the elastin protein consisting of an increase in polar' amino acids and a reduction in cross-linking amino acids. Subsequent treatment of lipoprotein-incubated arterial elastin with hot alkali and apolipoproteins did not reverse the binding of lipoprotein lipid to diseased elastin. INTRODUCTIONArterial elastic membranes appear to play an important role in the development of atherosclerotic plaques (1-9).In previous autoradiographic studies after intravenous injection of [8H] cholesterol (10), dense accumulations of radioactive cholesterol occurred on the split and fragReceived for publication 11 January 1972 and in revised form 15 June 1972. mented intimo-medial elastic membranes but not over collagen depositions in atherosclerotic plaques of all stages. These plaques included very small microscopic lesions which did not contain lipid in the cells of the slightly raised intima by autoradiography or lipid staining.Recent biochemical analyses of arterial elastin preparations have shown that the lipids accumulating on elastic membranes of atherosclerotic lesions are associated with the elastin protein of these elastic membranes, even in early atherosclerosis (11). The arterial elastin preparations were defined as that protein material which remained undegraded after alkali hydrolysis of arterial tissue homogenates. The studies suggest that arterial elastin is a protein-lipid complex with the lipids being bound to the elastin peptides. The composition of this protein-lipid complex is altered in elastin of atherosclerotic plaques. As compared with normal elastin, plaque elastin has a significantly higher content of polar amino acids and a significantly lower content of cross-linking amino acids. The alteration of plaque elastin protein is associated wi...

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“…suggested that the decrease in elastin concentration was in part due to increases of other components, such as collagen [88][89][90], while maintaining total elastin content [91]. It has also been shown that age could have altering effects on the amino acid structure of elastin.…”

Section: Effects Of Agementioning

confidence: 99%

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

Tsamis

Krawiec

Vorp

2013

J. R. Soc. Interface.

404

300

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Aortic disease is a significant cause of death in developed countries. The most common forms of aortic disease are aneurysm, dissection, atherosclerotic occlusion and ageing-induced stiffening. The microstructure of the aortic tissue has been studied with great interest, because alteration of the quantity and/or architecture of the connective fibres (elastin and collagen) within the aortic wall, which directly imparts elasticity and strength, can lead to the mechanical and functional changes associated with these conditions. This review article summarizes the state of the art with respect to characterization of connective fibre microstructure in the wall of the human aorta in ageing and disease, with emphasis on the ascending thoracic aorta and abdominal aorta where the most common forms of aortic disease tend to occur.

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Calcium and Elastin in Human Arteriosclerosis

Cited by 91 publications

References 0 publications

Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences

Age-related medial elastocalcinosis in arteries: mechanisms, animal models, and physiological consequences

The Interaction of Serum and Arterial Lipoproteins with Elastin of the Arterial Intima and Its Role in the Lipid Accumulation in Atherosclerotic Plaques

Elastin and collagen fibre microstructure of the human aorta in ageing and disease: a review

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