This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Hoff, H. F. Articles by Gaubatz, J. W. Search for Related Content PubMed PubMed Citation Articles by Hoff, H. F. Articles by Gaubatz, J. W.

Stroke, Vol 8, 366-370, Copyright © 1977 by American Heart Association

ARTICLES

Apolipoprotein B (apoB) retention in atherosclerotic intracranial arteries

HF Hoff, CL Heideman and JW Gaubatz

Low (LDL) and very low (VLDL) density lipoproteins retained in grossly normal and atherosclerotic human intracranial arteries have been quantitated using an electro-immunoassay directed against apolipoprotein B (apoB), the major protein of these two lipoprotein fractions. Buffer-homogenates of grossly normal arteries contained apoB amounts ranging from less than 0.04 to 1.58 microng/mg tissue dry weight, while those of atherosclerotic plaques gave values ranging from 0.80 to 3.9 microng per mg tissue dry weight. These results were consistent with immunofluorescence studies localizing apoB in these arteries. Plaques also contained a remaining fraction of tightly-bound apoB as evidenced by positive immunofluorescence in sections of pellets from buffer homogenates. This was in contrast to the negative results from grossly normal arteries. These results would suggest that retention of apoB by intracranial arteries correlates positively with vessel lesions. Arterial apoB is present in both grossly normal regions and plaques in a loosely-bound form, possibly representing intact lipoprotein. ApoB is also present in a tightly-bound form in plaques.