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Generation of Intracellular Signals by Low Density Lipoprotein Is Independent of the Classical LDL Receptor


Sachinidis, A; Locher, R; Vetter, W (1991). Generation of Intracellular Signals by Low Density Lipoprotein Is Independent of the Classical LDL Receptor. American Journal of Hypertension, 4(3 Pt 1):274-279.

Abstract

Low density lipoprotein cholesterol (LDL) and apolipoprotein B-100 (1 to 15 μg/mL) had no significant influence on the inositol-1,4,5-trisphosphate (InsPa) formation in vascular smooth muscle cells and fibroblasts. Low density lipoprotein cholesterol (15 μg/mL) induced an elevation of intracellular Ca2+ from 85 to approximately 210 nmol/L in vascular smooth muscle cells from rat aorta in the absence or in the presence of 15 μg/mL monoclonal antibodies against the classical low density lipoprotein receptor or in the presence of apolipoprotein B-100. Moreover, in both human cultured fibroblasts from normocholesterolemic individuals and from patients with familial hypercholesterolemia homozygote class 1, LDL induced a dose-dependent rise of free intracellular calcium and a biphasic change of intracellular pH. Since homozygote class 1 fibroblasts are classical LDL receptor negative, and as antibodies against this receptor, as well as apolipoprotein B-100, did not attenuate the LDL-induced elevation of cytosolic calcium, we conclude that LDL might modify vascular activity via the observed intracellular changes without involving the classical low density lipoprotein receptor. Am J Hypertens 1991;4:274-279

Abstract

Low density lipoprotein cholesterol (LDL) and apolipoprotein B-100 (1 to 15 μg/mL) had no significant influence on the inositol-1,4,5-trisphosphate (InsPa) formation in vascular smooth muscle cells and fibroblasts. Low density lipoprotein cholesterol (15 μg/mL) induced an elevation of intracellular Ca2+ from 85 to approximately 210 nmol/L in vascular smooth muscle cells from rat aorta in the absence or in the presence of 15 μg/mL monoclonal antibodies against the classical low density lipoprotein receptor or in the presence of apolipoprotein B-100. Moreover, in both human cultured fibroblasts from normocholesterolemic individuals and from patients with familial hypercholesterolemia homozygote class 1, LDL induced a dose-dependent rise of free intracellular calcium and a biphasic change of intracellular pH. Since homozygote class 1 fibroblasts are classical LDL receptor negative, and as antibodies against this receptor, as well as apolipoprotein B-100, did not attenuate the LDL-induced elevation of cytosolic calcium, we conclude that LDL might modify vascular activity via the observed intracellular changes without involving the classical low density lipoprotein receptor. Am J Hypertens 1991;4:274-279

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Item Type:Journal Article, refereed, original work
Communities & Collections:National licences > 142-005
Dewey Decimal Classification:Unspecified
Scopus Subject Areas:Health Sciences > Internal Medicine
Language:English
Date:1 March 1991
Deposited On:16 Oct 2018 15:00
Last Modified:15 Apr 2021 14:49
Publisher:Oxford University Press
ISSN:0895-7061
OA Status:Green
Publisher DOI:https://doi.org/10.1093/ajh/4.3.274

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