title: Effect of estradiol on low density lipoprotein uptake by bovine aortic endothelial cells.
abstract: The means by which estrogen retards atherosclerosis cannot be explained solely by changes in circulating lipoprotein levels. We studied the effects of 17 beta-estradiol on the binding, incorporation, and degradation of low density lipoprotein (LDL) by cultured bovine aortic endothelial cells (BAEC). Estrogen receptors in the cytoplasm and nucleus of BAEC could be demonstrated by immunofluorescent staining. Estradiol was found not to affect surface binding of LDL to BAEC. However, at physiologic concentrations (50 pg/ml), estradiol did enhance LDL uptake by the BAEC (P less than 0.005). This enhancement was present but somewhat reduced at higher concentrations of estrogen (P less than 0.05). Only approximately 10% of incorporated LDL was trichloroacetic acid soluble, indicating a low rate of LDL degradation. The relative rate of LDL breakdown within the BAEC was not altered by estrogen. These results, showing estrogen stimulation of LDL uptake by the BAEC, do not clarify the protective effect of this hormone. It is speculated that estrogen may augment the cellular clearance of LDL.
authors.affiliation: Case Western Reserve University School of Medicine, Cleveland, Ohio 44109.
authors.forename: J J
authors.initials: JJ
authors.lastname: Alexander
authors.forename: M
authors.initials: M
authors.lastname: Hoenig
authors.forename: D
authors.initials: D
authors.lastname: Graham
authors.forename: A
authors.initials: A
authors.lastname: Imbembo
mesh_terms: D000818:Animals; D001011:Aorta / Q000166:cytology / Q000378:metabolism*; D002417:Cattle; D002478:Cells, Cultured; D004730:Endothelium, Vascular / Q000166:cytology / Q000378:metabolism*; D004958:Estradiol / Q000494:pharmacology*; D005455:Fluorescent Antibody Technique; D008077:Lipoproteins, LDL / Q000378:metabolism*
chemical_list: D008077:Lipoproteins, LDL; D004958:Estradiol