JOE Society for Endocrinology Archive
HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


Journal of Endocrinology (1996) 151, 315-322       DOI: 10.1677/joe.0.1510315
© 1996 Society for Endocrinology
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Web of Science (21)
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Collins, A T
Right arrow Articles by Neal, D E
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Collins, A T
Right arrow Articles by Neal, D E

Benign prostatic stromal cells are regulated by basic fibroblast growth factor and transforming growth factor-β1

A T Collins, E J Robinson and D E Neal

The current study was undertaken, using cultures of prostatic epithelial and stromal cells, to determine the functional interactions between androgens, basic fibroblast growth factor (FGF2) and transforming growth factor-β1 (TGFβ1) and their importance in maintaining stromal homeostasis. Treatment of stromal cells with TGFβ1 significantly increased intracellular FGF2 and FGF2 sequestered to the extracellular matrix. FGF2 was also detected in stromal conditioned medium (SCM), but at levels 70-fold less than found in cell lysates. TGFβ1 (0·1 ng/ml) treatment caused an initial increase of 86% in secreted FGF2 levels, but high concentrations of TGFβ1 (5 ng/ml) decreased FGF2 levels by 38%, relative to the untreated control. Further studies showed that epithelial conditioned medium (ECM), androgen-treated, stromal conditioned medium (ASCM), but not SCM were mitogenic for stromal cells. Both ECM and ASCM caused a threefold increase in DNA synthesis. FGF2 may be the mediator of these interactions, since the mitogenic effect of both ECM and ASCM was significantly reduced by the addition of anti-FGF2 neutralising antibody. We hypothesise that the lack of response of stromal cells to SCM is due to TGFβ1 blocking the mitogenic effect of FGF2. Thus down-regulation of TGFβ1 synthesis, by androgens, results in stromal proliferation by ASCM.

Journal of Endocrinology (1996) 151, 315–322




This article has been cited by other articles:


Home page
Cancer Res.Home page
M. D. Heitzer and D. B. DeFranco
Hic-5/ARA55, a LIM Domain-Containing Nuclear Receptor Coactivator Expressed in Prostate Stromal Cells.
Cancer Res., July 15, 2006; 66(14): 7326 - 7333.
[Abstract] [Full Text] [PDF]


Home page
EndocrinologyHome page
D. C. Tomlinson, S. H. Freestone, O. C. Grace, and A. A. Thomson
Differential Effects of Transforming Growth Factor-{beta}1 on Cellular Proliferation in the Developing Prostate
Endocrinology, September 1, 2004; 145(9): 4292 - 4300.
[Abstract] [Full Text] [PDF]


Home page
CarcinogenesisHome page
Z. Li, T. Habuchi, N. Tsuchiya, K. Mitsumori, L. Wang, C. Ohyama, K. Sato, T. Kamoto, O. Ogawa, and T. Kato
Increased risk of prostate cancer and benign prostatic hyperplasia associated with transforming growth factor-beta 1 gene polymorphism at codon10
Carcinogenesis, February 1, 2004; 25(2): 237 - 240.
[Abstract] [Full Text] [PDF]




HOME HELP CONTACT US SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1996 by the Society for Endocrinology.