Interleukin-1 potentiation of β-endorphin secretion and the dynamics of interleukin-1 internalization in pituitary cells

Abstract

1. This study demonstrates that human recombinant Interleukin-1 (IL-1) stimulates β-endorphin release and potentiates the secretion of β-endorphin in both a mouse anterior pituitary cell line AtT-20 and rat pituitary cell cultures. 2. In pituitary cell cultures, prolonged treatment with phorbol ester had no effect on IL-1-induced β-endorphin release, but abolished the potentiating effects of IL-1 on vasopressin-induced β-endorphin secretion. 3. The enhancement of CRF-stimulated β-endorphin release by IL-1 was also reduced in normal pituitary cell cultures following depletion of protein kinase C. 4. The late IL-1-induced secretion of β-endorphin does not require the continuous presence of the cytpkine. 5. Incubation of monolayers with 125I-IL-1α (10 −9M) at 8°C and then at 37°C for various times revealed that IL-1α was internalized. There was a progressive increase in the ratio of cytoplasmic to cell-surface-associated 125I-IL-1α. 6. These results indicate that the IL-1-induced β-endorphin release and its potentiation of β-endorphin secretion involves internalization of this cytokine, perhaps via cell surface IL-1 receptors.