PMID- 8365375
OWN - NLM
STAT- MEDLINE
DCOM- 19931006
LR  - 20071114
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 133
IP  - 3
DP  - 1993 Sep
TI  - Transforming growth factor beta 1-like immunoreactivity in the pituitary gland of 
      the rat: effect of estrogen.
PG  - 1444-9
AB  - 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.
FAU - Burns, G
AU  - Burns G
AD  - Department of Veterinary and Comparative Anatomy, Pharmacology, and Physiology, 
      Washington State University, Pullman 99164-6520.
FAU - Sarkar, D K
AU  - Sarkar DK
LA  - eng
GR  - CA-56056/CA/NCI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Estrogens)
RN  - 0 (Transforming Growth Factor beta)
RN  - 9002-62-4 (Prolactin)
SB  - IM
MH  - Animals
MH  - Estrogens/*pharmacology
MH  - Female
MH  - Immunohistochemistry
MH  - Ovariectomy
MH  - Pituitary Gland, Anterior/chemistry/drug effects/*metabolism
MH  - Prolactin/analysis/metabolism
MH  - Rats
MH  - Rats, Inbred F344
MH  - Tissue Distribution
MH  - Transforming Growth Factor beta/analysis/*metabolism
EDAT- 1993/09/01 00:00
MHDA- 1993/09/01 00:01
CRDT- 1993/09/01 00:00
PHST- 1993/09/01 00:00 [pubmed]
PHST- 1993/09/01 00:01 [medline]
PHST- 1993/09/01 00:00 [entrez]
AID - 10.1210/endo.133.3.8365375 [doi]
PST - ppublish
SO  - Endocrinology. 1993 Sep;133(3):1444-9. doi: 10.1210/endo.133.3.8365375.