Aspirin induces alterations in low-density lipoprotein and decreases its catabolism by cultured human fibroblasts.
Aspirin interacts in vitro with human low-density lipoprotein (LDL), which results in a decrease in free amino groups of apolipoprotein B and an increase of electrophoretic mobility of the particle. The aspirin-treated LDL was less efficiently recognized than native LDL by the apo B/E receptor of fibroblasts. These results suggest that aspirin in long-term treatment could influence the LDL-receptor pathway. However, aspirin-treated LDL did not bind to the scavenger receptor of macrophages.
D000818:Animals; D001055:Apolipoproteins B / Q000378:metabolism; D001241:Aspirin / Q000494:pharmacology*; D001667:Binding, Competitive; D002460:Cell Line; D004586:Electrophoresis; D005347:Fibroblasts / Q000378:metabolism*; D006801:Humans; D005779:Immunodiffusion; D008077:Lipoproteins, LDL / Q000378:metabolism*; D008264:Macrophages / Q000378:metabolism; D051379:Mice; D011956:Receptors, Cell Surface / Q000378:metabolism; D011973:Receptors, LDL / Q000378:metabolism; D018110:Receptors, Lipoprotein
D001055:Apolipoproteins B; D008077:Lipoproteins, LDL; D011956:Receptors, Cell Surface; D011973:Receptors, LDL; D018110:Receptors, Lipoprotein; C032531:apolipoprotein B,E receptor; D001241:Aspirin