Age-Related Changes in Populations of Aortic Glycosaminoglycans

Species With Low Affinity for Plasma Low-Density Lipoproteins, and Not Species With High Affinity, Are Preferentially Affected

From the Departamento de Bioquímica Médica, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro (A.M.F.T., D.C.F.C., G.C.L., P.A.S.M.); and the Departamento de Patologia, Centro de Ciências Médicas, Universidade Federal Fluminense, Niterói (A.M.F.T.), Brazil.

Correspondence to Paulo A.S. Mourão, Departamento de Bioquímica Médica, Instituto de Ciências Biomédicas, Universidade Federal do Rio de Janeiro, Caixa Postal 68041, Rio de Janeiro, RJ, 21941–590, Brazil. E-mail mourao{at}server.bioqmed.ufrj.br

Abstract—Glycosaminoglycans were extracted from the intima and media layers of normal human thoracic aortas from donors of different ages. The arterial segments were devoid of macroscopically visible lesions obtained from patients who had no clinically evident cardiovascular disease. Total glycosaminoglycan content increases during the first 40 years of life. Changes in the content of hyaluronic acid and heparan sulfate are less noticeable. The content of chondroitin sulfate (mainly the 6-isomer) increases, whereas dermatan sulfate remains constant. Plasma LDL-affinity chromatography of dermatan sulfate+chondroitin 4/6-sulfate fractions allowed the separation of LDL high- and low-affinity glycosaminoglycan species. Remarkably, only glycosaminoglycan species with low affinity for plasma LDL increase with age in the disease-free areas of human thoracic aortas studied. These results suggest that age-related changes in glycosaminoglycan composition of the arterial wall do not contribute to increased deposition of plasma LDL. However, the alternative explanation that individuals with arterial glycosaminoglycans that avidly bind LDL would develop early and severe cardiovascular disease and would thus be excluded from our analysis cannot be ruled out.

Key Words: glycosaminoglycans • chondroitin sulfate • dermatan sulfate • atherosclerotic risk factor • LDL

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