In:
Acta Endocrinologica, Oxford University Press (OUP), Vol. 107, No. 2 ( 1984-10), p. 185-191
Abstract:
Abstract. The effect of phorbol diester tumour promoters on the release of growth hormone (GH) and prolactin (Prl) was studied in rat pituitary cells cultured in monolayer. 12- O -tetradecanoyl phorbol-13-acetate (TPA), the most potent phorbol ester, stimulated GH accumulation in the cultured medium in a dose-dependent manner. TPA also stimulated Prl accumulation. A time course study indicated that TPA mainly stimulates release of GH. The maximal stimulation of GH release by TPA (100 ng/ml) was 3–4-fold over control. Phorbol-12,13-dibutyrate (PDB), another tumour-promoting phorbol ester, stimulated GH release to an extent similar to that of TPA, while a biologically inactive compound, phorbol-12,13-diacetate (PDA), had no effect. TPA-stimulated GH release was not affected by the presence of indomethacin, an inhibitor of prostaglandin (PG) synthesis, indicating that PG is not involved in the process of TPA-stimulated GH release. Co ++ , a competitive antagonist of Ca ++ , at 2.0 m m completely suppressed the GH release induced by TPA, and this inhibition was partially reversed by the addition of 2.0 m m Ca ++ . Verapamil, a Ca ++ channel blocker, reduced TPA-stimulated GH release, and trifluoperazine, an inhibitor of Ca-calmodulin formation, had a similar effect. Somatostatin (SRIF) also inhibited the GH release by TPA. These observations are compatible with the idea that Ca ++ may be involved in the process of TPA-stimulated GH release. Since TPA has been reported to activate a Ca ++ - and phospholipiddependent protein kinase (protein kinase C), it is possible that TPA stimulate GH release by activating the enzyme. Further studies are required to clarify this point.
Type of Medium:
Online Resource
ISSN:
0804-4643
,
1479-683X
DOI:
10.1530/acta.0.1070185
Language:
Unknown
Publisher:
Oxford University Press (OUP)
Publication Date:
1984
detail.hit.zdb_id:
1485160-X
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