Cited by 101Lipid metabolism and disordersCholesterol and Lipid MetabolismLipoproteins and Cardiovascular Health

Lipoprotein lipase increases lipoprotein binding to the artery wall and increases endothelial layer permeability by formation of lipolysis products.

Rutledge, John C., Woo, Mable M., Rezai, Allen A., Curtiss, Linda K., Goldberg, Ira J.·1997·Circulation Research

Abstract

Mechanisms responsible for the accumulation of low-density lipoprotein (LDL) were investigated in a new model, the perfused hamster aorta. To do this, we developed a method to study LDL flux in real time in individually perfused arteries; each artery served as its own control. Using quantitative fluorescence microscopy, the rates of LDL accumulation and efflux were separately determined. Perfusion of arteries with buffer plus lipoprotein lipase (LpL) increased LDL accumulation 5-fold (0.1 +/- 0.03 mV/min [control] versus 0.5 +/- 0.05 mV/min [LpL]) by increasing LDL retention in the artery wall. This effect was blocked by heparin and monoclonal antibodies directed against the amino-terminal region of apolipoprotein B (apo B). This suggests that specific regions of apo B are involved in LDL accumulation within arteries. Also, the effect of hydrolysis of triglyceride-rich lipoproteins on endothelial barrier function was studied. We compared endothelial layer permeability using a water-soluble reference molecule, fluorescently labeled dextran. When LpL was added to hypertriglyceridemic plasma, dextran accumulation within the artery wall increased > 4-fold (0.024 +/- 0.01 mV/min [control] versus 0.098 +/- 0.05 mV/min [LpL]). Under the same conditions, LpL increased LDL accumulation approximately 3-fold (0.016 +/- 0.003 mV/min [control] versus 0.047 +/- 0.013 mV/min [LpL]). Rapid efflux of LDL from the artery wall indicated that increased endothelial layer permeability was the primary mechanism during periods of increased lipolysis. Our data demonstrate two LpL-mediated effects that may increase the amount of LDL in the artery wall. These findings may pertain to the observed relationship between increased postprandial lipemia and atherosclerosis.

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Crossref · 10.1161/01.res.80.6.819

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Authors
Rutledge, J. C., Woo, M. M., Rezai, A. A., Curtiss, L. K., & Goldberg, I. J.
Affiliations
Scripps Research Institute (US)
Venue
Circulation Research
Published
1997-06
Volume
80
Issue
6
Pages
819-828
ISSN
  • 0009-7330 (ISSN-L)
  • 1524-4571
OpenAlex
W2101670650
Cited by
101
References
48
Citations by year
2026: 1 · 2025: 3 · 2024: 1 · 2021: 2 · 2020: 1 · 2019: 1 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 1 · 2014: 2 · 2013: 1 · 2012: 3
FWCI
5.60
Type
journal article
Language
en
Open access
closed
Locations
  • Circulation Research (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5p50hl021006-17)
  • National Heart, Lung, and Blood Institute (HL55667, HL45095, HL 21006, R01HL055667)
Topics
  • Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Lipid metabolism and disorders
  • Health Sciences › Medicine › Surgery › Cholesterol and Lipid Metabolism
  • Health Sciences › Medicine › Surgery › Lipoproteins and Cardiovascular Health
Keywords
lipoprotein lipase, apolipoprotein B, lipolysis, endothelial permeability, triglyceride-rich lipoproteins, hypertriglyceridemia, postprandial lipemia, atherosclerosis, heparin, monoclonal antibodies
MeSH terms
Animals, Arteries, Capillary Permeability, Endothelium, Vascular, Cricetinae, Lipolysis, Lipoprotein Lipase, Lipoproteins, Lipoproteins, LDL, Mesocricetus, Microscopy, Fluorescence

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