Endocrinology, Vol 133, 1444-1449, Copyright © 1993 by Endocrine Society

ARTICLES

Transforming growth factor beta 1-like immunoreactivity in the pituitary gland of the rat: effect of estrogen

G Burns and DK Sarkar
Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, Washington State University, Pullman 99164-6520.

We have recently shown that transforming growth factor-beta 1 (TGF beta 1) is produced in the rat pituitary gland and inhibits the secretion of PRL and the estrogen-induced growth of lactotropes. In this study, we sought to ascertain whether TGF beta 1 inhibits lactotropic functions by an autocrine or paracrine mechanism. Our techniques consisted of localizing the pituitary distribution of the growth factor immunoreactivity and measuring changes in pituitary TGF beta 1 and PRL levels in the presence and absence of estrogen in ovariectomized animals. With the use of standard immunohistochemical techniques, we observed that in cyclic females and ovariectomized rats, 60 +/- 7% of the cells exhibiting TGF beta 1-like immunoreactivity in the anterior pituitary were lactotropes. In addition, the melanotropes in the intermediate lobe appeared to be TGF beta 1 immunopositive. Treatment with estrogen for 7 days reduced the number of TGF beta 1- immunoreactive lactotropes. Immunoreactive TGF beta 1 was also detectable in anterior pituitary extracts using a specific RIA. Estrogen treatment decreased the level of TGF beta 1 in the anterior pituitary extracts from ovariectomized rats. TGF beta 1 immunoreactivity was inversely proportional to the overall size of the anterior pituitary and the concentrations of PRL, as measured in both the anterior lobe extracts and plasma. These results suggest that lactotropes may serve as a site of TGF beta 1 synthesis and that the production of TGF beta 1 in these cells can be negatively influenced by PRL stimulation through the action of the lactotrope-proliferating hormone, estrogen. Furthermore, these data support the notion that TGF beta 1 controls lactotropic function by an autocrine mechanism.

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