TRANSFORMING GROWTH FACTOR-BETA(1)-LIKE IMMUNOREACTIVITY IN THE PITUITARY-GLAND OF THE RAT - EFFECT OF ESTROGEN

We have recently shown that transforming growth factor-beta1 (TGFbeta1) 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 TGFbeta1 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 TGFbeta1 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 TGFbeta1-like immunoreactivity in the anterior pituitary were lactotropes. In addition, the melanotropes in the intermediate lobe appeared to be TGFbeta1 immunopositive. Treatment with estrogen for 7 days reduced the number of TGFbeta1-immunoreactive lactotropes. Immunoreactive TGFbeta1 was also detectable in anterior pituitary extracts using a specific RIA. Estrogen treatment decreased the level of TGFbeta1 in the anterior pituitary extracts from ovariectomized rats. TGFbeta1 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 TGFbeta1 synthesis and that the production of TGFbeta1 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 TGFbeta1 controls lactotropic function by an autocrine mechanism.