RPG: Regulation of Prolactin Gene Expression by Cell Contacts

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9507173 Delidow Regulation of pituitary prolactin (PRL) gene expression involves the actions of a number of neurotransmitters, hormones, growth factors and other soluble signaling molecules. In addition it has been shown that changes in extracellular matrix components can regulate PRL gene expression, and that agents which regulate PRL can also induce changes in cell adhesiveness. Preliminary data has shown that PRL gene expression in the rat pituitary tumor 235-1 cells is induces under culture conditions in which large cell aggregates form, and that high PRL mRNA levels are dependent upon the presence of these aggregates. To persue these observations, the proposed research will attempt to: 1. Determine by cell culture studies whether induction of PRL gene expression requires contact with aggregates, or whether a soluble factor(s) is produced by aggregates and acts independently of cell contact. If the signal appears to be a soluble factor, aggregate-conditioned media will be assayed for the ability to induce PRL mRNA. 2. Determine by agonist/inhibitor studies whether the signal is transduced via cellular kinase pathways. Actin and tubulin staining will be used to examine changes in cytoskeletal organization. The presence of beta1-integrins, cadherins and neural cell adhesion molecules will also be determined. 3. Determine whether the increase in PRL mRNA occurs at the transcriptional level. These studies will provide a base of information for future studies on contact regulation of PRL gene expression. ***