Advertisement

Regulation of Cyclooxygenase Synthesis in Vascular Smooth Muscle Cells by Epidermal Growth Factor

  • J. Martyn Bailey
  • Timothy Hla
  • Barbara Muza
  • James Pash
Part of the GWUMC Department of Biochemistry Annual Spring Symposia book series (GWUN)

Abstract

The prostaglandin synthases, which are widely distributed throughout the various organ systems of the body, are activated primarily by release of substrate arachidonic acid from cellular phospholipids (Hamberg et al., 1975). These prostaglandin-synthesizing systems may become refractory to further challenge by arachidonic acid substrate because of a self-inactivating feature of the cyclooxygenase enzyme first characterized by Smith and Lands (1972). This is mediated by free-radical intermediates of the reaction, which permanently inactivate the enzyme. An analogous refractoriness also develops following exposure to aspirin (Vane, 1971) and is caused by acetylation of a serine residue in the active site (Roth et al., 1975).

Keywords

Epidermal Growth Factor Arachidonic Acid Vascular Smooth Muscle Cell Confluent Culture Aspirin Treatment 
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. Bailey, J.M., Bryant, R.W., Whiting, J., and Salata, K., 1983, Characterization of 11-HETE and 15-HETE, together with prostacyclin, as major products of the cyclooxygenase pathway in cultured rat aorta smooth muscle cells, J. Lipid Res. 24:1419–1428.PubMedGoogle Scholar
  2. Bailey, J.M., 1980, Regeneration of prostacyclin synthase activity in cultured vascular cells following aspirin treatment, Adv. Prostaglandin Thromboxane Res. 6:537–541.PubMedGoogle Scholar
  3. Hamberg, M., Svensson, J., and Samuelsson, B., 1975, Thromboxanes: A new group of biologically active compounds derived from prostaglandin endoperoxides, Proc. Nad. Acad. Sci. U.S.A. 72:2994–2998.CrossRefGoogle Scholar
  4. Moncada, S., Herman, A.G., Higgs, E.A., and Vane, J.R., 1977, Differential formation of prostacyclin (PGX or PGI2) by layers of the arterial wall. An explanation for the antithrombotic properties of vascular endothelium, Thromb. Res. 11:323–344.PubMedCrossRefGoogle Scholar
  5. Ross, R., and Glomset, J.A., 1976, The pathogenesis of atherosclerosis, N. Engl. J. Med. 295:369–377.PubMedCrossRefGoogle Scholar
  6. Roth, G.J., Stanford, N., and Majerus, P.W., 1975, Acetylation of prostaglandin synthase by aspirin, Proc. Natl. Acad. Sci. U.S.A. 72:3073–3076.PubMedCrossRefGoogle Scholar
  7. Smith, W.L., and Lands, W.E.M., 1972, Oxygenation of polyunsaturated fatty acids during prostaglandin biosynthesis by sheep vesicular gland, Biochemistry 11:3276–3285.PubMedCrossRefGoogle Scholar
  8. Vane, J.R., 1971, Inhibition of prostaglandin synthesis as a mechanism of action for aspirin-like drugs, Nature (New Biol.) 231:232–235.Google Scholar
  9. Weksler, B.B., 1983, Differential inhibition by aspirin or vascular and platelet prostaglandin synthesis in atherosclerotic patients, N. Engl. J. Med. 308:800–805.PubMedCrossRefGoogle Scholar
  10. Whiting, J., Salata, K., and Bailey, J.M., 1980, Aspirin: An unexpected side effect on prostaglandin synthesis in cultured vascular smooth muscle cells, Science 210:663–665.PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1985

Authors and Affiliations

  • J. Martyn Bailey
    • 1
  • Timothy Hla
    • 1
  • Barbara Muza
    • 1
  • James Pash
    • 1
  1. 1.Department of BiochemistryGeorge Washington University School of Medicine and Health SciencesUSA

Personalised recommendations