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Related Experiment Videos

Apolipoprotein E and lipoprotein lipase increase triglyceride-rich particle binding but decrease particle penetration

Adam E Mullick1, Richard J Deckelbaum, Ira J Goldberg

  • 1Division of Endocrinology, University of California, Davis 95616, USA. aemullick@ucdavis.edu

Arteriosclerosis, Thrombosis, and Vascular Biology
|December 17, 2002
PubMed
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Apolipoprotein E (apoE) and lipoprotein lipase (LpL) increase triglyceride-rich particle (TGRP) accumulation in arteries but block their penetration, suggesting a novel antiatherogenic mechanism.

Area of Science:

  • Cardiovascular Biology
  • Lipid Metabolism
  • Atherosclerosis Research

Background:

  • Liver-derived apolipoprotein E (apoE) is known to reduce atherosclerosis.
  • The role of apoE and lipoprotein lipase (LpL) in arterial wall interactions of triglyceride-rich particles (TGRPs) is not fully understood.

Purpose of the Study:

  • To evaluate the effects of apoE and LpL on TGRP interactions within the arterial wall.
  • To investigate the potential antiatherogenic properties of apoE and LpL.

Main Methods:

  • Quantitative fluorescence microscopy was employed to study TGRP interactions in rat carotid arteries.
  • Arteries were perfused with fluorescently labeled TGRPs in the presence or absence of apoE and LpL.

Main Results:

Related Experiment Videos

  • TGRP accumulation in the arterial wall increased by 220% with apoE and 100% with LpL.
  • Both apoE and LpL significantly reduced the deep penetration of TGRPs into the arterial wall.
  • Heparin attenuated the TGRP accumulation effect.

Conclusions:

  • ApoE and LpL enhance TGRP accumulation in the arterial wall.
  • Crucially, apoE and LpL inhibit TGRP penetration into the arterial wall.
  • This dual action may represent a novel antiatherogenic mechanism for apoE and LpL.