Role of Mucoid Substances of the Aorta in the Deposition of Lipids

Gerö, S; Gergely, J.; Devenyi, T; Jakab, L; Székely, Judit; Virág, S

doi:10.1038/187152a0

Cited by 62 publications

(3 citation statements)

References 4 publications

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“…However, even among those who broadly accept this hypothesis, there have been significant differences concerning the mechanism of retention of lipid at these sites. For example, in relation to arteries it has been suggested that lipid deposition in the intima (a) is due to arrested filtration of plasma through the vessel wall, because of blockage of fenestrations in the elastic lamina (Gofman and Young, 1963), giving rise to one form of " plasmatic vasculosis " (Lendrum, 1964, cited by Adams, 1967; (b) arises because plasma lipid is " dammed-back " in the intima secondary to medial changes, such as enzyme defects due to anoxia (Adams, Bayliss and Ibrahim, 1962;Adams) or scarring of the muscular coat (Wilens and McCluskey, 1954); (c) occurs because of a selective retention of large molecular weight proteins owing to a '' molecular sieving " effect of the subendothelial connective-tissue gel (Adams); (d) results from interaction of plasma LDL with the AMPS of the arterial wall (Amenta and Waters, 1960;Gero et al, 1960;Walton and Williamson).…”

Section: Significance Of Lipid Deposition In Mitral and Aortic Valvesmentioning

confidence: 99%

The pathogenesis of atherosclerosis of the mitral and aortic valves

Walton

Williamson

Johnson

1970

The Journal of Pathology

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Section: Significance Of Lipid Deposition In Mitral and Aortic Valvesmentioning

confidence: 99%

The pathogenesis of atherosclerosis of the mitral and aortic valves

Walton

Williamson

Johnson

1970

The Journal of Pathology

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“…The role of the ground substance in the aorta has been reviewed, especially its affinity for lipids as an initial atherogenic factor (27, 28). The accumulation of ground substance in the aorta has been confirmed in atherosclerosis (29), dissecting aneurysm (30) and cystic medionecrosis (31).…”

Section: Discussionmentioning

confidence: 99%

Aortic Medial Calcification in Progeria‐Like Syndrome†

Ishii

1977

J American Geriatrics Society

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Aortic medial calcification was investigated in rats in which the progeria-like syndrome (PLS) was evoked by administering dihydrotachysterol. In 35 experimental rats and 15 controls, calcification was studied morphologically by light and electron microscopy, and by enzyme histochemistry. Body weight, food intake and serum calcium levels were also determined. Calcification occurred along and on the elastic lamellae in association with the accumulation of ground substance. In the smooth-muscle cells surrounding the calcified foci, the activities of various lysosomal enzymes increased concomitantly with a tendency toward transformation of smooth-muscle cells to a modified form. From these observations, the role of ground-substance formation by smooth-muscle cells is postulated, and participation in the catabolism of ground substance by the lysosomal enzymes of these cells is suggested. It appears the increased activity of adenosine monophosphatase should be linked to the calcification. The etiology of weight loss, skin manifestations and aortic calcification in PLS rats seems to be different from that in human progeric diseases. Therefore, the PLS rat should not be readily accepted as an animal model for the study of progeric diseases.

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“…Since the early experiments by Gero et al (1960), a great deal of data were published suggesting that aortic GAGs contribute to the deposition of lipids in the atherosclerotic lesions by insolubilizing lipoproteins (Bihari-Varga et al, 1981;Camejo, 1982).…”

Section: Interaction Of Pgs With Hyaluronic Acidmentioning

confidence: 99%

Proteoglycans from pig aorta. Comparative study of their interactions with lipoproteins

Wegrowski¹,

Moczar²,

Robert³

1986

Biochemical Journal

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Different proteoglycans (PGs) were isolated from pig aorta for aggregation studies with hyaluronic acid and human low-density lipoproteins (LDL). Extraction of the intima-media with 4M-guanidinium chloride and digestion of the residue with collagenase solubilized 91 % of aortic hexuronic acid content. From the guanidinium chloride extract two PGs were isolated by ion-exchange and gel-permeation chromatography: proteochondroitin sulphate (PGI) with a protein-core apparent Mr of 250000 and proteodermatanchondroitin sulphate (PGII) with a protein-core apparent Mr of 55000. Only PGI forms high-Mr aggregates with hyaluronic acid. From the collagenase digest two other PGs were isolated: proteoheparan sulphate and proteochondroitin sulphate (PGIII and PGIV respectively). PGIV had a smaller hydrodynamic size than PGI. PGI and PGII formed insoluble complexes with human LDL in the presence of Ca2 . PGIII or PGIV did not form precipitates with the LDL. PGI and PGII, but neither PGIII nor PGIV, were bound to LDL-Sepharose. The main peaks of PGI and PGII were eluted from LDL-Sepharose with 60 mm-and 90 mM-NaCl respectively. The results indicate that aortic PGs have different interacting potentials with lipoproteins, depending on their Mr and their glycosaminoglycan composition.

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Role of Mucoid Substances of the Aorta in the Deposition of Lipids

Cited by 62 publications

References 4 publications

The pathogenesis of atherosclerosis of the mitral and aortic valves

The pathogenesis of atherosclerosis of the mitral and aortic valves

Aortic Medial Calcification in Progeria‐Like Syndrome†

Proteoglycans from pig aorta. Comparative study of their interactions with lipoproteins

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