Arterial uptake and synthesis of low density lipoproteins.
The accumulation of cholesterol in atherosclerotic lesions is associated with an increased uptake of plasma cholesterol and LDL by the arterial wall. During the regression of atherosclerosis, the uptake of these macromolecules returns to or below normal, suggesting that the retention of cholesterol in regressed lesions is due to a defect in the removal of cholesterol from the arterial wall rather than to an abnormality in vascular permeability. Although increased amounts of 125I-LDL were detected in atherosclerotic vessels, the percent distribution and fractional degradation rate of 125I-LDL appeared similar in normal and diseased vessels. The present studies in support of earlier findings in human vessels indicate that LDL in the artery is contained in a number of different cellular and extracellular pools in close association with AMPS. These lipoproteins appeared to be derived not only from the lipoproteins contained in the plasma but also from lipoproteins synthesized by the arterial wall.
D000818:Animals; D001011:Aorta / Q000378:metabolism; D001158:Arteries / Q000378:metabolism*; D001161:Arteriosclerosis / Q000378:metabolism*; D002784:Cholesterol / Q000097:blood / Q000378:metabolism; D004036:Diet, Atherogenic; D000882:Haplorhini; D008077:Lipoproteins, LDL / Q000096:biosynthesis / Q000378:metabolism*; D008252:Macaca fascicularis; D008297:Male; D009130:Muscle, Smooth / Q000378:metabolism
D008077:Lipoproteins, LDL; D002784:Cholesterol