Human venous and arterial glycosaminoglycans have similar affinity for plasma low-density lipoproteins

• Published in: Biochimica et biophysica acta 2002-04, Vol.1586 (3), p.243-253
• Main Authors: Leta, Graziela C, Mourão, Paulo A.S, Tovar, Ana M.F
• Format: Article
• Language: English
• Subjects: Adult; Aorta, Thoracic; Arteries; Chemical Fractionation; Chondroitin sulfate; Chondroitin Sulfates - analysis; Chromatography, Affinity; Chromatography, Ion Exchange; Dermatan sulfate; Dermatan Sulfate - analysis; Electrophoresis, Polyacrylamide Gel; Glycosaminoglycan; Glycosaminoglycans - blood; Glycosaminoglycans - chemistry; Glycosaminoglycans - metabolism; Humans; Lipoprotein; Lipoproteins, LDL - blood; Lipoproteins, LDL - metabolism; Low-density lipoprotein; Middle Aged; Saphenous Vein; Varicose Veins - metabolism
• ISSN: 0925-4439; 0006-3002; 1879-260X
• DOI: 10.1016/S0925-4439(01)00102-8

We compared the glycosaminoglycan content of human venous and arterial walls. The most abundant glycosaminoglycan in human veins is dermatan sulfate whereas chondroitin 4/6-sulfate is preponderant in arteries. The concentrations of chondroitin 4/6-sulfate and heparan sulfate are ∼4.8- and ∼2.5-fold higher in arteries than in veins whereas dermatan sulfate contents are similar in the two types of blood vessels. Normal and varicose saphenous veins do not differ in their glycosaminoglycan contents. It is known that certain glycosaminoglycan species from the arterial wall, mainly high-molecular-weight fractions of dermatan sulfate+chondroitin 4/6-sulfate have greater affinity for plasma LDL. These types of glycosaminoglycans can be identified on a LDL-affinity column. We now demonstrated that a similar population of glycosaminoglycan also occurs in veins, although with a lower concentration than in the arteries due to less chondroitin 4/6-sulfate with affinity for LDL. The concentrations of dermatan sulfate species, which interact with LDL, are similar in arteries and veins. The presence of these glycosaminoglycans with affinity to plasma LDL in veins raises interesting questions concerning the role of these molecules in the pathogenesis of atherosclerosis. Possibly, the presence of these glycosaminoglycans in the vessel wall are not sufficient to cause retention of LDL and consequently endothelial dysfunction, but may require additional intrinsic factors and/or the hydrodynamic of the blood under the arterial pressure.