Studies on the passage of plasma proteins across arterial endothelium in relation to atherogenesis.
Previous studies using isotopically labelled lipoproteins or immuno-histological characterisation of the apolipoproteins present in atherolsclerotic lesions have suggested that lipoproteins varying in size from LDL to VLDL gain entry to the lesions. It has also been shown that a fraction of these lipoproteins is firmly bound to various constituents of the arterial wall. Using the immunoperoxidase technique at the electron microscopic level, it is now confirmed that spherical molecules specifically interacting with labelled anti-LDL (anti-apolipoprotein B) and of a range of molecular diameters corresponding to those of LDL to VLDL are indentifiable in the intersitial matrix of lesions. The labelled antibodies also identified lipoprotein bound to elastin, within smooth muscle cells, and bound to collagen fibres. In advanced lesions lipoprotein was found to be bound not only to "normal" (native) collagen fibrils but also with a characteristic periodicity to fibrous long-spacing collagen. The occurrence of this "abnormal" form of collagen in plaques is now reported for the first time but its possible significance in relation to atherogenesis is discussed.
D000328:Adult; D001158:Arteries / Q000378:metabolism* / Q000648:ultrastructure; D001161:Arteriosclerosis / Q000378:metabolism* / Q000473:pathology; D001798:Blood Proteins / Q000378:metabolism*; D003094:Collagen / Q000378:metabolism; D004727:Endothelium / Q000378:metabolism; D005260:Female; D006801:Humans; D007124:Immunoenzyme Techniques; D008074:Lipoproteins / Q000378:metabolism; D008077:Lipoproteins, LDL / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D009130:Muscle, Smooth / Q000378:metabolism; D010539:Permeability
D001798:Blood Proteins; D008074:Lipoproteins; D008077:Lipoproteins, LDL; D003094:Collagen