Fluid-Phase Pinocytosis in Arterial Smooth Muscle Cells

  • D. E. Bowyer
  • E. M. Muir
Conference paper

Abstract

Pinocytosis is the process by which cells take up materials from the extracellular environment. This can involve the specific recognition of a macromolecule by a receptor on the plasma membrane, followed by the interiorisation of the receptor-ligand complex (receptor-mediated pinocytosis, or the non-specific uptake of material present in the fluid entrapped within the forming pinosomes (non-specific fluid-phase pinocytosis). The functions of these processes include the uptake of nutrients and hormones, and possibly membrane surveillance. They may also be of significance in the pathological-overload of cells with extracellular substances. In atherosclerosis overload of arterial smooth muscle cells (SMC) with lipid, predominantly cholesterol and cholesteryl esters, is a characteristic feature of the foam cell (1). SMC take up low density lipoprotein (LDL) by both receptor-mediated and non-specific fluid-phase pinocytosis (2). Uptake by the receptor-mediated pathway, however, leads to the down regulation of receptors. It has been calculated that even under normal conditions, the concentrations of LDL to which SMC are exposed, would cause maximal suppression of the LDL receptor. Under such conditions the non-specific route may contribute significantly to the uptake of LDL (3). This route would become even more important under conditions in which the concentration of lipoproteins in the interstitial fluid is raised, for example hypercholesterolemia or following loss of the endothelium. In view of the potential significance of the fluid-phase pathway in atherogenesis we have developed a method for its measurement in arterial SMC in culture, investigated the basic mechanisms involved, and begun to explore ways in which it may be modified.

Keywords

Cholesterol Sucrose Foam Fluoride Choline 

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References

  1. 1.
    Coltoff-Schiller B, Goldfischer, S, Adamany AM, Wolinsky, H (1976) Endocytosis by vascular smooth muscle in vivo and in vitro. Am J Path 83: 45–60Google Scholar
  2. 2.
    Goldstein JL, Brown MS (1977) The low density lipoprotein pathway and its relation to atherosclerosis.Ann Rev Biochem 46: 897–930PubMedCrossRefGoogle Scholar
  3. 3.
    Goldstein JL, Brown MD (1977) Atherosclerosis: the low density lipoprotein receptor hypothesis. Metabolism 26: 1257–1275PubMedCrossRefGoogle Scholar
  4. 4.
    Muir EM (1981) Ph.D Thesis (Cambridge University)Google Scholar
  5. 5.
    Laake DS, Bowyer DE (1977) Quantitative studies of pinocytic uptake of 125 I-labelled PVP by pig aortic smooth muscle cells in culture. Biochem Soc 5: 130–133Google Scholar
  6. 6.
    Pozzan T, Corps AN, Pontecurro CM, Hesketh TR, Metcalfe JC (1980) Cap formation by various ligands on lymphocytes shows the same dependence on high cellular ATP levels. Biochim Biophys Acta 602: 558–566PubMedCrossRefGoogle Scholar
  7. 7.
    Alien RD (1975) Evidence for firm linkages between microtubules and membrane bounded vesicles. J Cell Biol 64: 497–503CrossRefGoogle Scholar
  8. 8.
    Duncan R, Pratten MK (1971) Membrane economics in endocytic systems. J Theor Biol 66: 729–739Google Scholar
  9. 9.
    Davies PF, Ross R (1978) Mediation of pinocytosis in cultured arterial smooth muscle cells and endothelial cells by platelet derived growth factor. J Cell Biol 79: 663–671PubMedCrossRefGoogle Scholar
  10. 10.
    Mahoney EM, Hamill AL, Scott WA, Cohn ZA (1977) Response of endocytosis to altered fatty acyl composition of macrophage phospholipid. Proc Natl Acad Sci USA 74: 4895–4899PubMedCrossRefGoogle Scholar
  11. 11.
    Samochowiec L, Kadibowska D, Rozewicka L, Kuza W, Szysska R (1976) Investigations in experimental atherosclerosis Part 2: the effect of phosphatidylcholine (EPL) in experimental changes in miniature pigs. Atherosclerosis 23: 319–331CrossRefGoogle Scholar
  12. 12.
    Bowyer DE, Fox JW, Muir EM (1979) Hemmung der endozytose in arteriellen glatten muskelzellen durch hochungesattigtes phosphatidylcholin. Med Welt 30: 1447–1448PubMedGoogle Scholar
  13. 13.
    Pagano RE, Weinstein JN (1978) Interactions of liposomes with mammalian cells. A Rev Biophys Bioeng 7: 435–468CrossRefGoogle Scholar
  14. 14.
    Niinikoski J, Heughan C, Hunt TK (1973) Oxygen tensions in the aortic wall of normal rabbits Atherosclerosis 17: 353–359PubMedCrossRefGoogle Scholar
  15. 15.
    Roberts AVS, Nicholls SDE, Williams KT, Lloyd JB (1976) Pinocytosis and intracellular proteolysis in experimentally induced lysosomal storage. Biochem Soc Trans 2: 1096–1098Google Scholar
  16. 16.
    Stein O, Halperin C, Stein Y (1979) Comparison of cholesterol egress from cultured cells enriched with cholesteryl ester after exposure to cationised LDL and chloroquine. Biochim Biophys Acta 573: 1–11PubMedGoogle Scholar
  17. 17.
    Stauber WT, Trout JJ, Schottelius BA (1981) Exocytosis of intact lysosomes from skeletal muscle after chloroquine treatment. Exp mol Path 34: 87–93CrossRefGoogle Scholar
  18. 18.
    Maxfield FR, Davies PJA, Klempner L, Willingham ML, Pastan (1979) Epidermal growth factor stimulation of DNA synthesis is potentiated by compounds that inhibit its clustering in coated pits. Proc Natl Acad Sci USA 76: 5731–5735PubMedCrossRefGoogle Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1983

Authors and Affiliations

  • D. E. Bowyer
  • E. M. Muir

There are no affiliations available

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