PMID- 1480172
OWN - NLM
STAT- MEDLINE
DCOM- 19930210
LR  - 20181130
IS  - 0888-8809 (Print)
IS  - 0888-8809 (Linking)
VI  - 6
IP  - 11
DP  - 1992 Nov
TI  - Transforming growth factor-beta 1 messenger RNA and protein expression in the 
      pituitary gland: its action on prolactin secretion and lactotropic growth.
PG  - 1825-33
AB  - Transforming growth factor-beta 1 (TGF-beta 1) is known to inhibit cell growth 
      and proliferation of many estrogen-responsive normal and transformed cells. The 
      effect of this polypeptide growth factor on the estrogen-responsive pituitary 
      lactotropes has not been determined. To evaluate the role of TGF-beta 1 in the 
      control of lactotropic growth, the action and production of TGF-beta 1 in the 
      anterior pituitary was studied in rats. The growth factor suppressed basal PRL 
      release from the primary culture of enriched rat lactotropes in a 
      concentration-dependent manner in the range of 2 pg/ml-20 ng/ml. The growth 
      factor did not affect the secretion of other pituitary hormones in the cultures. 
      The inhibitory action of TGF-beta 1 on PRL release was time dependent. The 
      minimum time required to produce a significant effect was 4 h. The growth factor 
      also suppressed estradiol-induced PRL release as well as it inhibited 
      estradiol-induced proliferation of lactotropes. TGF-beta 1 immunoreactivity was 
      detected in the cellular extracts of cultured anterior pituitary cells and in the 
      extracts of anterior pituitary tissue. In addition, the primary culture of 
      enriched rat lactotropes secreted TGF-beta 1. Using Northern blot techniques, a 
      2.4-kilobase transcript of pro-TGF-beta 1 mRNA was detected both in the anterior 
      pituitary tissue and in the primary culture of anterior pituitary cells. These 
      data suggest that TGF-beta 1 is produced in the pituitary gland and inhibits the 
      secretion of PRL and growth of lactotropes in an autocrine and/or paracrine 
      fashion.
FAU - Sarkar, D K
AU  - Sarkar DK
AD  - Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, 
      Washington State University, Pullman 99164.
FAU - Kim, K H
AU  - Kim KH
FAU - Minami, S
AU  - Minami S
LA  - eng
GR  - AG-05453/AG/NIA NIH HHS/United States
GR  - CA56056/CA/NCI NIH HHS/United States
GR  - ORR05465-27/OR/ORS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Mol Endocrinol
JT  - Molecular endocrinology (Baltimore, Md.)
JID - 8801431
RN  - 0 (Recombinant Fusion Proteins)
RN  - 0 (Transforming Growth Factor beta)
RN  - 4TI98Z838E (Estradiol)
RN  - 9002-62-4 (Prolactin)
SB  - IM
MH  - Animals
MH  - Cell Division/drug effects
MH  - Cells, Cultured
MH  - Depression, Chemical
MH  - Estradiol/pharmacology
MH  - Female
MH  - Gene Expression
MH  - Ovariectomy
MH  - Pituitary Gland, Anterior/cytology/*metabolism
MH  - Prolactin/*metabolism
MH  - Rats
MH  - Rats, Inbred F344
MH  - Recombinant Fusion Proteins/pharmacology
MH  - Secretory Rate/drug effects
MH  - Transforming Growth Factor beta/*biosynthesis/genetics/physiology
EDAT- 1992/11/01 00:00
MHDA- 1992/11/01 00:01
CRDT- 1992/11/01 00:00
PHST- 1992/11/01 00:00 [pubmed]
PHST- 1992/11/01 00:01 [medline]
PHST- 1992/11/01 00:00 [entrez]
AID - 10.1210/mend.6.11.1480172 [doi]
PST - ppublish
SO  - Mol Endocrinol. 1992 Nov;6(11):1825-33. doi: 10.1210/mend.6.11.1480172.