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Low‐density lipoproteins induce the polar secretion of PAI‐1 by endothelial cells in culture
Author(s) -
Jovin Ion S.,
Willuweit Antje,
Taborski Uwe,
Lehnhardt Andreas,
Schreiner Karin,
Klövekorn WolfPeter,
MüllerBerghaus Gert
Publication year - 2003
Publication title -
american journal of hematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.456
H-Index - 105
eISSN - 1096-8652
pISSN - 0361-8609
DOI - 10.1002/ajh.10314
Subject(s) - secretion , compartment (ship) , chemistry , umbilical vein , plasminogen activator , medicine , lumen (anatomy) , plasminogen activator inhibitor 1 , basal (medicine) , cell culture , endocrinology , biology , in vitro , microbiology and biotechnology , biochemistry , oceanography , genetics , insulin , geology
Patients with hypercholesterolemia and with coronary atherosclerosis have increased plasma levels of plasminogen activator inhibitor (PAI)‐1. PAI‐1 and low‐density lipoproteins (LDL) are also present in the walls of atherosclerotic vessels, where they participate in the development and remodeling of the atherosclerotic plaques. We investigated the influence of LDL on the apical (luminal) and basolateral (subendothelial) secretion of PAI‐1 by human umbilical vein endothelial cells in a two‐compartment cell‐culture model. Confluent cells were incubated with LDL either in the apical compartment or in the basal compartment. Cells incubated with culture medium served as controls. A significantly higher concentration of PAI‐1 was found in both the apical ( P = 0.025) and the basal compartment ( P = 0.025) if cells were incubated with LDL on the basolateral side. In contrast, incubation of the cells with LDL apically resulted in an increased PAI‐1 concentration only in the apical compartment ( P = 0.028) and not in the basal compartment. Our findings indicate that the LDL particles that reach the subendothelial space can induce an increased release of PAI‐1 by endothelial cells into the vessel lumen and also contribute to the release of PAI‐1 into the subendothelial space and thus to the process of atherosclerotic plaque remodeling. Am. J. Hematol. 73:66–68, 2003. © 2003 Wiley‐Liss, Inc.