Functional Differentiation and its Regulation in Pituitary Cells.

Abstract

It has been an interesting problem to understand why specific hormones are produced from specific cells. It is known that in the human anterior pituitary gland, tumors are classified into those of growth hormone (GH), prolactin (PRL). ACTH, thyroid stimulating hormone (TSH), and gonadotrophin secreting adenomas as well as nonfunctioning adenomas. In human pituitary adenomas, GH secreting adenoma is usually plurihormonal, i. e., the adenoma not only produces GH but also PRL and TSH. TSH secreting adenoma is also plurihormonal, and adenoma produces TSH as well as GH and PRL. Thus, it was supposed that common transcriptional factors participate in the functional differentiation of GH, PRL, and TSH. Pit-1 has been proposed to regulate GH, PRL, and TSH cells and the dwarf mutants in mice were produced by Pit-1 gene mutations. Simmons et al. (1990) observed Pit-1 protein expression in GH, PRL, and TSH cells [10], in the adult rat pituitary gland although Pit-1 mRNA expression was observed in all cell types (Fig. 1). Therefore it was anticipated that, in human pituitary tumors, the functional expression in GH and TSH secreting adenomas may be under the regulation of Pit-1 protein. We describe here the overview of transcriptional factors depicted by immunohistochemistry and in situ hybridization.