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This version published online on November 6, 2003
Endocrinology, doi:10.1210/en.2003-1063
A more recent version of this article appeared on February 1, 2004
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Submitted on August 15, 2003
Accepted on October 27, 2003

Involvement of PKC-dependent MAP kinase p44/42 signaling pathway for cross-talk between estradiol and TGF-{beta}3 in increasing bFGF in folliculostellate cells

KIRTI CHATURVEDI1 and DIPAK K. SARKAR1*

1 Endocrinology Program, Biomedical Division of the Center of Alcohol Studies and Department of Animal Sciences, Rutgers, The State University of New Jersey, 84 Lipman Drive, New Brunswick, NJ 08901

* To whom correspondence should be addressed. E-mail: sarkar{at}aesop.rutgers.edu.

We have recently shown that transforming growth factor-beta3 (TGF-{beta}3), in the presence of estradiol, increases the release of basic fibroblast growth factor (bFGF) from folliculostellate (FS) cells in the pituitary. We determined the interactive effects of TGF-{beta}3 and estradiol on bFGF production and release from FS cells, and the role of the mitogen-activated protein (MAP) kinase pathway in TGF-{beta}3 and estradiol interaction. We found that TGF-{beta}3 and estradiol alone moderately increased cell content and release of bFGF from FS cells, but together they markedly increased the peptide. Estradiol and TGF-{beta}3 alone moderately activated MAP kinase p44/42; together they produced marked activation of MAP kinase p44/42. Pretreatment of FS cells with an MEK1/2 inhibitor or with protein kinase C (PKC) inhibitors suppressed the activation of MAP kinase p44/42, bFGF release, and protein level increases, all of which were induced by TGF-{beta}3 and estradiol. Estradiol and TGF-{beta}3, either alone or in combination, increased the levels of active Ras. Furthermore, bFGF induction by TGF-{beta}3 and estradiol was blocked by over-expression of Ras N17, a dominant negative mutant of Ras p21. Estrogen receptor blocker ICI 182,780 failed to prevent estrogen's and TGF-{beta}3's effects on bFGF. These data suggest that an estradiol receptor-independent PKC-activated Ras-dependent MAP kinase pathway is involved in the cross-talk between TGF-{beta}3 and estradiol to increase bFGF production and/or release from FS cells.
Key words: TGF-{beta}3 • estradiol • bFGF • folliculostellate cells • lactotrope growth control




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