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Related Experiment Videos

Lipoprotein lipase can function as a monocyte adhesion protein

J C Obunike1, S Paka, S Pillarisetti

  • 1Department of Medicine, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.

Arteriosclerosis, Thrombosis, and Vascular Biology
|July 1, 1997
PubMed
Summary

Lipoprotein lipase (LPL) enhances monocyte adhesion to surfaces by bridging cell surface proteoglycans. This interaction, independent of lipase activity but partly mediated by integrins, may increase macrophage accumulation in arteries.

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Area of Science:

  • Biochemistry
  • Cell Biology
  • Immunology

Background:

  • Lipoprotein lipase (LPL) is found in atherosclerotic lesions and binds to cell surface heparan sulfate proteoglycans (HSPGs).
  • Cell surface HSPGs are known to mediate cell adhesion to proteins.

Purpose of the Study:

  • To investigate if LPL binding to HSPGs mediates monocyte adhesion to surfaces.
  • To explore the mechanisms underlying LPL-mediated monocyte adhesion.

Main Methods:

  • Assessing monocyte binding to LPL-coated surfaces and LPL-treated subendothelial matrix.
  • Using enzymatic treatments (heparinase, heparitinase) and inhibitors (heparin, tetrahydrolipstatin, RGD peptides) to probe binding mechanisms.
  • Investigating the role of HSPGs and integrins in LPL-mediated monocyte adhesion.

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Main Results:

  • LPL significantly increased monocyte binding to tissue culture plates, subendothelial matrix, and endothelial cells.
  • Monocyte binding to LPL was reduced by heparinase/heparitinase treatments and heparin, indicating HSPG involvement.
  • Monocyte binding to LPL was partially inhibited by RGD peptides, suggesting integrin involvement.
  • LPL lipase activity inhibition did not affect monocyte binding.

Conclusions:

  • LPL dimers act as a bridge, mediating monocyte adhesion through interactions with both matrix and monocyte surface HSPGs.
  • Monocyte binding to LPL involves both HSPGs and, in part, monocyte cell surface integrins.
  • LPL-augmented monocyte adhesion may contribute to macrophage accumulation in arteries, a key process in atherosclerosis.