title: Distribution patterns of apolipoproteins A1, A2, and B in the wall of atherosclerotic vessels.
abstract: Atherosclerotic vessels were analysed histochemically for distribution, quantity, and composition of apolipoprotein (Apo) types in the vascular wall. The specimens comprised all stages of atherosclerosis, from very discrete intimal changes to complicated lesions. The vessel specimens were marked with antibodies against human Apo A1, A2, and B. Apo A1 can be demonstrated in even the earliest stage of atherosclerosis, and increases with the progression of the disease. In the initial stage, Apo A1 is found first in lumen-adjacent layers of the intima, and is evident in deeper layers of the wall as the disease progresses. Arteries of muscular type show accumulation of Apo in an earlier stage (or in greater quantity at the same stage) than arteries of elastic type. At all stages, the amount of Apo A1 always exceeds that of A2 and B. In the intima, Apo B is higher than Apo A2, the media contains hardly any Apo B, and the adventitia has less B than A2. Within the intimal layer, Apo A1 and A2 are found in an intracellular (mainly in foam cells) or in an extracellular location, according to the stage of atherosclerosis. Apo B is almost exclusively extracellular; only cases of advanced atherosclerosis show some intracellular localization (mostly in foam cells), visualized as electron dense lamellar organelles, probably of lysosomal origin. In the media, Apo A1 and A2 are accumulated in intracellular deposits, whereas the extracellular storage of Apo A1, A2 and B is observed only in cases with the most severe damage. Our investigations suggest that the accumulation of apolipoproteins in the vascular wall is affected not only by insudation from the plasma, but also by neosynthesis and/or metabolism by locally derived cells or cells immigrating in the process of atherosclerosis. The presence of Apo A1 and A2 in the vessel wall is now documented, and their role at this site apparently differs from that in the plasma.
authors.affiliation: Gerhard-Domagk-Institut für Pathologie, Münster, Federal Republic of Germany.
authors.forename: E
authors.initials: E
authors.lastname: Vollmer
authors.forename: J
authors.initials: J
authors.lastname: Brust
authors.forename: A
authors.initials: A
authors.lastname: Roessner
authors.forename: A
authors.initials: A
authors.lastname: Bosse
authors.forename: F
authors.initials: F
authors.lastname: Burwikel
authors.forename: B
authors.initials: B
authors.lastname: Kaesberg
authors.forename: B
authors.initials: B
authors.lastname: Harrach
authors.forename: H
authors.initials: H
authors.lastname: Robenek
authors.forename: W
authors.initials: W
authors.lastname: Böcker
mesh_terms: D001011:Aorta / Q000737:chemistry* / Q000473:pathology; D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D001054:Apolipoproteins A / Q000032:analysis*; D001055:Apolipoproteins B / Q000032:analysis*; D001161:Arteriosclerosis / Q000378:metabolism* / Q000473:pathology; D003331:Coronary Vessels / Q000737:chemistry* / Q000473:pathology; D006801:Humans
chemical_list: D016632:Apolipoprotein A-I; D016633:Apolipoprotein A-II; D001054:Apolipoproteins A; D001055:Apolipoproteins B