Abstract
In 1979, we first reported that in order to inhibit prostaglandin (PG) synthesis, anti-inflammatory steroids required glucocorticoid receptor occupancy, ribonucleic acid (RNA) and new protein synthesis (Russo-Marie et al., 1979). As it had been previously demonstrated that steroids were inhibiting PG synthesis by inhibiting the release of arachidonic acid from their membrane phospholipid stores, probably by inhibiting the enzyme responsible for the phospholipid deacylation (Gryglewski et al., 1975; Hong & Levine, 1976), we advanced the hypothesis that this induced protein was able to inhibit phospholipase A2. In the meantime, Flower & Black-well (1979) reported also that anti-inflammatory steroids induced the biosynthesis of a phospholipase A2 inhibitor which prevents prostaglandin generation. In the model they used, they were able to demonstrate that the protein was not only induced but was also released by the cell which had been synthesizing it.
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References
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© 1984 Macmillan Publishers Limited
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Rothhut, B., Russo-Marie, F., Cousin, M., Lando, D. (1984). Renocortin: a phospholipase A2 inhibitory protein induced by anti-inflammatory steroids: pharmacological and biological properties, development of monoclonal antibodies. In: Paton, W., Mitchell, J., Turner, P. (eds) IUPHAR 9th International Congress of Pharmacology. Palgrave, London. https://doi.org/10.1007/978-1-349-86029-6_7
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DOI: https://doi.org/10.1007/978-1-349-86029-6_7
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