Connective tissue responses to oxysterols

doi:10.1016/0021-9150(82)90190-3

Atherosclerosis

Volume 41, Issues 2–3, February 1982, Pages 255-266

https://doi.org/10.1016/0021-9150(82)90190-3 Get rights and content

Abstract

We studied the effect of sterols and oxidized sterols on promoting tissue inflammation and necrosis, and on causing cell death in tissue culture. The cells studied were mouse fibroblasts and macrophages, and pig vascular smooth muscle. The lipid preparations were dibromide-purified cholesterol, air-oxidized cholesterol, 25-hydroxycholesterol, cholesterol-5α,6β-epoxide and cholestane-3β,5α,6β-triol. Of these, the triol was most active in its cytopathic effect on cells in culture, in size of granuloma formation and in producing necrosis. The epoxide, 25-hydroxycholesterol and air-oxidized cholesterol produced rather less effect on tissues and cultures than the triol, but more than purified cholesterol and the control. The results are considered in relation to the presence of oxysterols in stored foodstuffs and their possible presence over the surface of cholesterol crystals in the tissues.

References (24)

M.S. Brown et al.
Suppression of 3-hydroxy-3-methyl-glutaryl CoA reductase activity and inhibition of growth of human fibroblasts by 7-keto-cholesterol
J. Biol. Chem.
(1974)
O.B. Bayliss High et al.
The role of macrophages and giant cells in advanced human atherosclerosis
Atherosclerosis
(1980)
J. Folch et al.
A simple method for the isolation and purification of total lipides from animal tissues
J. Biol. Chem.
(1957)
F. Snyder
Radioassay of thin-layer chromatograms — A high resolution zonal scraper for quantitative C¹4 and H³ scanning of thin-layer chromatograms
Analyt. Biochem.
(1964)
L.L. Smith et al.
Sterol metabolism, Part 9 (26-Hydroxycholesterol levels in the human aorta)
Atherosclerosis
(1970)
L.L. Smith et al.
Sterol metabolism, Part 18 (On the uniqueness of the occurrence of 26-hydroxycholesterol in the human aorta)
Atherosclerosis
(1973)
C.B. Taylor et al.
Spontaneously occurring angiotoxic derivatives of cholesterol
Amer. J. Clin. Nutr.
(1979)
P. Constantinides
Plaque fissures in human coronary thrombosis
J. Atheroscler. Res.
(1966)
D.M. Spain et al.
Rabbit local tissue response to triglycerides, cholesterol, and its ester
Arch. Path.
(1962)
C.W.M. Adams et al.
Phospholipids in atherosclerosis — The modification of the cholesterol granuloma by phospholipids
J. Path. Bact.
(1963)

Y.H. Abdulla et al.

Connective-tissue reactions to implantation of purified sterols, sterol esters, phosphoglycerides, glycerides and free fatty acids

J. Path. Bact.

(1967)

W.A. Harland et al.

Tissue reaction to atheroma lipids

J. Path.

(1973)

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^☆: This work was partly supported by a grant from the British Heart Foundation.

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Research paperConnective tissue responses to oxysterols☆

Abstract

J. Biol. Chem.

Atherosclerosis

J. Biol. Chem.

Analyt. Biochem.

Atherosclerosis

Atherosclerosis

Amer. J. Clin. Nutr.

J. Atheroscler. Res.

Rabbit local tissue response to triglycerides, cholesterol, and its ester

Arch. Path.

Phospholipids in atherosclerosis — The modification of the cholesterol granuloma by phospholipids

J. Path. Bact.

Connective-tissue reactions to implantation of purified sterols, sterol esters, phosphoglycerides, glycerides and free fatty acids

J. Path. Bact.

Tissue reaction to atheroma lipids

J. Path.

Research paper
Connective tissue responses to oxysterols☆