These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Transforming growth factor-beta 1 messenger RNA and protein expression in the pituitary gland: its action on prolactin secretion and lactotropic growth.
    Author: Sarkar DK, Kim KH, Minami S.
    Journal: Mol Endocrinol; 1992 Nov; 6(11):1825-33. PubMed ID: 1480172.
    Abstract:
    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.
    [Abstract] [Full Text] [Related] [New Search]