Advertisement

Interaction of Platelets, Macrophages and Lipoproteins in Relation to Atherogenes

  • A. J. Day
  • S. Preet Singh
  • K. Hudson
  • S. Mojumder
Conference paper

Abstract

Both macrophages and platelets have been considered as key cells in the cellular pathology of atherosclerosis for many years. Their suggested role however has been progressively modified as experimental data has emerged. Recent studies for example, have demonstrated the presence of receptors to modified LDL in macrophages (1,2) and have renewed early interest (3,4) in the reticuloendothelial system in the formation of foam cells in early atherogenesis. Recent interest in platelets has centred on the involvement on prostacyclin and thromboxane on platelet aggregation and on the effect of platelet growth factors in the proliferation of arterial wall cells (5,6). There are a number of studies however which suggest that platelets might also promote cellular lipid accumulation and foam cell formation in the early lesion. Platelet thrombi injected in vivo stimulate the formation of macrophage foam cells (7,8). Where endothelial injury occurs (either by indwelling catheters or by repeated ballooning) platelet deposition is followed by the development of lipid containing cell lesions (9,10) with composition and metabolic characteristics of early atherogenesis (11). In the present study the interaction of platelets on various aspects of lipid uptake and metabolism in rabbit peritoneal macrophages is studied in vitro and some preliminary data on possible mechanisms for platelet involvement in foam cell formation suggested.

Keywords

Cholesteryl Ester Foam Cell Formation Cholesterol Acyl Transferase Subsequent Uptake Macrophage Foam Cell 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Goldstein J.L., Ho Y.K., Basu S.K. and Brown M.S. (1979) Binding site on macrophages that mediates uptake and degradation of acetylated low density lipoprotein, producing massive cholesterol deposition. Proc Natl Acad Sci USA 76: 333–337PubMedCrossRefGoogle Scholar
  2. 2.
    Goldstein J.L., Ho Y.K., Brown M.S., Innerarity T.L. and Mahley R.W. (1980) Cholesteryl ester accumulation in macrophages resulting from receptor-mediated uptake and degradation of hypercholesterolemic canine — β-very low density lipoproteins. J Biol Chem 255: 1839–1848PubMedGoogle Scholar
  3. 3.
    Day A.J. (1964) The macrophage system, lipid metabolism and atherosclerosis. J Atheroscler Res 4: 117–130PubMedCrossRefGoogle Scholar
  4. 4.
    Day A.J. (1967) Lipid metabolism by macrophages and its relationship to atherosclerosis. In “Advances in Lipid Research” (Ed. R. Paoletti and D. Kritchevsky) Academic Press 5: 185–207Google Scholar
  5. 5.
    Gryglewski R.J., Deminska-Kiec A., Zmuda A and Gryglewska T. (1978) Prostacyclin and thromboxane A2 biosynthesis capacities of heart, arteries and platelets at various stages of experimental atherosclerosis in rabbits. Atherosclerosis 31: 385–394PubMedCrossRefGoogle Scholar
  6. 6.
    Ross R., Glomset J.A., Kariya B. and Harker L.A. (1974) A platelet-dependent serum factor that stimulates the proliferation of arterial smooth muscle cells in vitro. Proc Natl Acad Sci USA 71: 1207–1210PubMedCrossRefGoogle Scholar
  7. 7.
    Chandler A.B. and Hand R.A. (1961) Phagocytized platelets; a source of lipids in human thrombi and atherosclerotic plaques. Science 134: 946–947PubMedCrossRefGoogle Scholar
  8. 8.
    Ardlie N.G. and Schwartz C.J. (1968) The organization and fate of autologous pulmonary emboli in hypercholesterolaemic rabbits. J Path & Bact 95: 19–28CrossRefGoogle Scholar
  9. 9.
    Moore S. (1979) Endothelial Injury and Atherosclerosis. Exp Mol Pathol 31: 182–190PubMedCrossRefGoogle Scholar
  10. 10.
    Minick C.R., Stemerman M.B. and Insull, W. (1977) Effect of regenerated endothelium on lipid accumulation in the arterial wall. Proc Natl Acad Sci USA 74: 1724–1728PubMedCrossRefGoogle Scholar
  11. 11.
    Day A.J., Bell F.P., Moore S. and Friedman R. (1974) Lipid composition and metabolism of thrombo-atherosclerotic lesions produced by continued endothelial damage in normal rabbits. Circulation Res 34: 467–476PubMedGoogle Scholar
  12. 12.
    Fogelman A.M., Schechter I., Seager J., Hokom M., Child J.S. and Edwards P.A. (1980) Maiondialdehyde alteration of low density lipoproteins leads to cholesteryl ester accumulation in human monocyte-macrophages. Proc Natl Acad Sci USA 77: 2214–2218PubMedCrossRefGoogle Scholar
  13. 13.
    Day A.J. and Fidge N.H. (1962) The uptake and metabolism of C14-labelled fatty acids by macrophages in vitro. J Lipid Res 3: 333–338Google Scholar
  14. 14.
    Brecher P. and Chan C.T. (1980) Properties of acyl-CoA: cholesterol O-Acyl transferase in aortic microsomes from atherosclerotic rabbits. Biochim Biophys Acta 617: 458–471PubMedGoogle Scholar
  15. 15.
    Brecher P., Pyun H.Y. and Chobanian A.V. (1977) Effect of atherosclerosis on lysosomal cholesterol esterase activity in rabbit aorta. J Lipid Res 18: 154–163PubMedGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1983

Authors and Affiliations

  • A. J. Day
  • S. Preet Singh
  • K. Hudson
  • S. Mojumder

There are no affiliations available

Personalised recommendations