Low density lipoproteins transfer bacterial lipopolysaccharides across endothelial monolayers in a biologically active form.
Open Access
- 1 February 1988
- journal article
- research article
- Published by American Society for Clinical Investigation in Journal of Clinical Investigation
- Vol. 81 (2), 601-605
- https://doi.org/10.1172/jci113359
Abstract
Rabbit aortic endothelial cells (RAECs) were grown on micropore filters in a device that allowed in situ determination of transendothelial electrical resistance (TEER). Incubation of confluent RAEC monolayers with 2 ng.ml-1 of bacterial LPS for 3 h did not change the protein content or the number of cells on the filters, but resulted in a marked decline in TEER (from 14.1 +/- 0.9 to 5.1 +/- 0.6 omega.cm2) and a significant increase in LDL transport across the monolayers (from 154 +/- 13 to 456 +/- 41 ng. h-1 per cm2). In contrast, exposure of RAEC monolayers for 3 d to as much as 5 micrograms.ml-1 of LPS complexed to LDL (LPS-LDL) did not alter the TEER or LDL transport. LPS-LDL was transported across the monolayers at the same rate as LDL. While microgram quantities of LPS complexed to LDL did not disrupt the integrity of the endothelial monolayer, incubation of RAECs with transported LPS-LDL at concentrations of 25-100 ng LPS.ml-1 resulted in a two- to ninefold increase in the secretion of monocyte chemotactic activity by these cells. Incubation of rabbit aortic smooth muscle cells with transported LPS-LDL at concentrations of 25-100 ng LPS.ml-1 resulted in a two- to threefold increase in the secretion of monocyte chemotactic activity. We propose that LDL protects endothelial cells from the acute toxicity of LPS but the resulting complexes are transported across the endothelium in a biologically active form that can initiate an inflammatory response.This publication has 26 references indexed in Scilit:
- Rabbit beta-migrating very low density lipoprotein increases endothelial macromolecular transport without altering electrical resistance.Journal of Clinical Investigation, 1986
- Monocyte chemotactic factor produced by large vessel endothelial cells in vitro.Arteriosclerosis: An Official Journal of the American Heart Association, Inc., 1986
- Control of monocyte recruitment by chemotactic factor(s) in lesion-prone areas of swine aorta.Arteriosclerosis: An Official Journal of the American Heart Association, Inc., 1985
- Studies of hypercholesterolemia in the nonhuman primate. I. Changes that lead to fatty streak formation.Arteriosclerosis: An Official Journal of the American Heart Association, Inc., 1984
- New function for high density lipoproteins. Their participation in intravascular reactions of bacterial lipopolysaccharides.Journal of Clinical Investigation, 1979
- The preparation and characterization of a radioiodinated bacterial lipopolysaccharideImmunochemistry, 1978
- Scanning electron microscopy: Morphology of aortic endothelium following injury by endotoxin and during subsequent repairAtherosclerosis, 1977
- Endotoxin-induced vascular endothelial injury and repair: II. Focal injury, en face morphology, [3H]thymidine uptake and circulating endothelial cells in the dogExperimental and Molecular Pathology, 1976
- The metabolism of very low density lipoprotein proteins I. Preliminary in vitro and in vivo observationsBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, 1972
- THE DISTRIBUTION AND CHEMICAL COMPOSITION OF ULTRACENTRIFUGALLY SEPARATED LIPOPROTEINS IN HUMAN SERUMJournal of Clinical Investigation, 1955