Cholestan-3gb,5α,6β-triol decreases barrier function of cultured endothelial cell monolayers
Reference (25)
- et al.
Cytotoxicity of oxidation derivatives of cholesterol on cultured aortic smooth muscle cells and their effect on cholesterol biosynthesis
Am. J. Clin. Nutr.
(1979) - et al.
Cholesterol oxidation derivatives and arterial endothelial damage
Atherosclerosis
(1985) - et al.
Distribution of 25-hydroxycholesterol in plasma lipoproteins and its role in atherogenesis
Atherosclerosis
(1982) - et al.
Spontaneously occurring angiotoxic derivatives of cholesterol
Am. J. Clin. Nutr.
(1979) - et al.
Inhibition of protein synthesis blocks the response to 25-hydroxycholesterol by inhibiting degradation of hydroxymethylglutaryl CoA reductase
Biochim. Biophys. Acta
(1982) - et al.
Radioimmune precipitation of 3-hydroxy-3-methylglutaryl coenzyme A reductase from Chinese hamster fibroblasts
J. Biol. Chem.
(1981) - 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) - et al.
The formation of echinocytes by the insertion of oxygenated sterol compounds into red cell membranes
Blood
(1980) - et al.
Alteration of86Rb+ influx and efflux following depletion of membrane sterol in L-cells
J. Biol. Chem.
(1978) - et al.
Endothelial permeability: pathways and modulations
Ann. N.Y. Acad. Sci.
(1982)
Hyperlipidemia and atherosclerosis. Chronic hyperlipidemia initiates and maintains lesions by endothelial cell desquamation and lipid accumulation
Science
Lipid composition of rabbit aortic wall following removal of endothelium by balloon catheter
Arteriosclerosis
Cited by (48)
Phospholipid packing defects and oxysterols in atherosclerosis: Dietary prevention and the French paradox
2019, BiochimieCitation Excerpt :Since then, Korahani et al. have reported auto-oxidation of cholesterol in the solid state under conditions similar to food processing and cooking [33], and Staprans et al. found that adding oxidized cholesterol to a diet fed to rabbits increased atherosclerotic lesions in rabbit aortas by 100% [34]. In the 1980s, Henning and Boissonneault investigated the hypothesis that the vascular endothelial barrier function could be altered by cholesterol oxidation products [35]. The researchers tested the effects of added cholesterol and the oxysterol cholestan-3β,5α,6β-triol (Triol) on albumin transfer across monolayers of cultured vascular endothelial cells.
Inflammation at the blood-brain barrier: The role of liver X receptors
2017, Neurobiology of DiseaseCitation Excerpt :Since the 90s, several studies describe a role for oxysterols in LXR activations in peripheral endothelial cell (dys)function. These studies demonstrated an elevation in endothelial permeability for albumin, i.e. decreased barrier function, across vascular endothelial monolayers after exposure to oxysterols (Hennig and Boissonneault, 1987; Ramasamy et al., 1992). Furthermore, oxysterol incubation of human umbilical vein endothelial cells (HUVECs) resulted in alterations in the activity of membrane-bound enzymes leading to increased calcium influx and endothelial cell toxicity (Ramasamy et al., 1992; Zhou et al., 2000).
Cholesterol attenuates linoleic acid-induced endothelial cell activation
2003, Metabolism: Clinical and ExperimentalCitation Excerpt :Considering the amount of serum (5% to 10%) present in our culture media and albumin being the vehicle for introducing solubilized cholesterol, concentrations of 25 to 100 μmol/L were chosen. We have also shown that endothelial cell exposure to such concentrations results in cellular cholesterol enrichment and that levels of up to 100 μmol/L are nontoxic to the vascular endothelium.21 The cells were scraped in 1 mL of phosphate-buffered saline (PBS) to which was added 3 times the volume of hexane:isopropanol (3:2), which was then vortexed and incubated at room temperature for 30 minutes.