Roles of Lipases in the Development of Autonomic Neurons

  • Fusao Hirata
  • Toshio Hattori
  • Yoshitada Notsu
  • Bernd Hamprecht
Conference paper
Part of the FIDIA Research Series book series (FIDIA, volume 4)

Abstract

Glucocorticoids are widely used as therapeutics for immunological and inflammatory diseases (Sayers and Travis, 1970). This anti-inflammatory action of glucocorticoids is now proposed to be associated with the inhibition of the release of arachidonic acid, a precursor of inflammatory agents such as prostaglandins and leukotrienes (Blackwell et al., 1978). Arachidonic acid is mostly present in an esterified form rather than as a free fatty acid. Thus, the rate limiting step of the arachidonate release from intact cells is the activation of phospholipase A2 or phospholipase C. Furthermore, this anti-inflammatory action of glucocorticoids can be blocked by the previous treatment with cycloheximide and actinomycin D, inhibitors of protein and RNA syntheses, respectively (Hirata et al., 1985b). From these observations, one can assume that glucocorticoids induce the synthesis of a protein(s) which inhibits cellular phospholipases. Recently, the four groups (Flower’s group in England, Russo-Marie’s group in France, and Goldberg’s group and our group in USA) have partially purified and characterized such a factor(s) and named this protein as lipocortin (DiRosa et al., 1984). Isolated lipocortin can suppress the carageenin-induced paw edema, an animal model of acute inflammation, and can inhibit the release of arachidonic acid from various intact cells. Thus, it has been proposed that the inhibition of phospholipases A2 by lipocortin might be the main mechanism of the anti-inflammatory action of glucocorticoids (Hirata et al., 1985b).

Keywords

Arachidonic Acid HL60 Cell Superior Cervical Ganglion Fluocinolon Acetonide Tyrosine Hydroxylase Activity 
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. Black IB, Adler JE, Dreytus CF, Jonakeit GM, Katz DM, LaGamma EF, Markey KM (1984) Neurotransmitter plasticity at the molecular level. Science 225: 1266–1270.PubMedCrossRefGoogle Scholar
  2. Blackwell GJ, Flower RJ, Nikamp FP, Vane JR (1978) Phospholipase A2 activity of guinea pig isolated perfused lungs: Stimulation and inhibition by anti-inflammatory steroids. Brit J Pharmacol 62: 78–79.CrossRefGoogle Scholar
  3. DiRosa M, Flower RJ, Hirata F, Parente L, Russo-Marie F (1984) Letter to the editor; Anti-phospholipase proteins, Nomenclature announcement. Prostaglandins 28: 441–442.CrossRefGoogle Scholar
  4. Hattori T, Hirata F, Hoffman T, Hizuta A, Herberman RB (1983) Inhibition of human natural killer (NK) activity and antibody dependent cellular cytotoxicity (ADCC) by lipomodulin, a phospholipase inhibitory protein. J Immunol 131: 662–665.PubMedGoogle Scholar
  5. Heumann R, Ocalan M, Hamprecht B (1979) Factors from glial cells regulate choline acetyltransferase and tyrosine hydroxylase activities in a hybrid-hybrid cell line. FEBS Letters 107: 37–41.PubMedCrossRefGoogle Scholar
  6. Hirata F (1985) Molecular mechanisms on the modulation of phospholipid metabolism by glucocorticoids. In: Bailey M (ed): Prostaglandins, Leukotrienes and Lipoxins; Biochemistry, Mechanism of action and clinical application, Plenum, New York; pp. 119–123.CrossRefGoogle Scholar
  7. Hirata F, Matsuda K, Wano Y, Hattori T (1985a) The biochemical mechanism of cellular activation. Int J Immunopharmacol, in press.Google Scholar
  8. Hirata F, Notsu Y, Yamada R, Ishihara Y, Wano Y, Kunos I, Kunos G (1985b) Isolation and characterization of lipocortin (lipomodulin). Agents and Action, 17: 263–266.CrossRefGoogle Scholar
  9. Iwata M, Akasaki M, Ishizaka K (1984) Modulation of the biological activities of IgE binding factor. VI The activation of phospholipase by glycosylation enhancing factor. J Immunol 133: 1505–1512.PubMedGoogle Scholar
  10. McEwin BS (1979) Influences of adreno-cortical hormones on pituitary and brain functions. In: Baxter JD, Rosseau GG (eds): Glucocorticoid hormone action. Springer-Verlag, Berlin, Heidelberg and New York, pp. 449–465.Google Scholar
  11. Nirenberg M, Wilson S, Higashida H, Rotter A, Krueger K, Busis N, Ray R, Kenimer JF, Adler M (1983) Modulation of synapse formation by cyclic adenosine monophosphate. Science 222: 794–799.PubMedCrossRefGoogle Scholar
  12. Notsu Y, Namiuchi S, Hattori T, Matsuda K, Hirata F (1985) Inhibition of phospholipases by Met-Leu-Phe-Ile-Leu-Ile-Lys-Arg-Ser-Arg-His-Phe, C terminus of middle-sized tumor antigen. Arch Biochem Biophys 236: 195–204.PubMedCrossRefGoogle Scholar
  13. Patterson PH (1978) Environmental determination of autonomic neurotransmitter functions. Ann Rev Neurosci 1: 1–17.PubMedCrossRefGoogle Scholar
  14. Sayers G, Travis RH (1970) Adrenocorticotropic hormones: Adrenocortical steroids and their synthetic analogs. In: Goodman LS, Gilman A (eds): Pharmacological basis of therapeutics. McMillan, New York, pp. 1604–1642.Google Scholar

Copyright information

© Springer-Verlag Berlin Heidelberg 1986

Authors and Affiliations

  • Fusao Hirata
    • 1
  • Toshio Hattori
    • 1
  • Yoshitada Notsu
    • 1
  • Bernd Hamprecht
    • 2
  1. 1.Laboratory of Cell BiologyNational Institute of Mental HealthBethesdaUSA
  2. 2.Physiologisch-Chemisches Institut der Universität87 WurzburgWest Germany

Personalised recommendations