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J. Biol. Chem., Vol. 275, Issue 28, 21653-21660, July 14, 2000
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From the The mechanisms that control the emergence of
different anterior pituitary cells from a common stem cell population
are largely unknown. The immortalized GHFT cells derived from targeted
expression of SV40 T antigen to mouse pituitary display characteristics
of somatolactotropic progenitors in that they express the transcription factor GHF-1 (Pit-1) but not growth hormone (GH) or prolactin (PRL). We
searched for factors capable of inducing lactotropic differentiation of
GHFT cells. PRL gene expression was not observed in cells
subjected to a variety of stimuli, which induce PRL gene expression in mature lactotropes. Only fibroblast growth factor-2 (FGF-2) was able to initiate the transcription, synthesis, and release
of PRL in GHFT cells. However, induction of PRL expression was incomplete in FGF-2-treated cells, suggesting that additional factors are necessary to attain high levels of PRL
transcription in fully differentiated lactotropes. We also show that
the FGF-2 response element is located in the proximal PRL
promoter. Stimulation of PRL expression by FGF-2 requires
endogenous Ets factors and these factors as well as GHF-1 are expressed
at low levels in the committed precursor, suggesting that these low
levels are limiting for full PRL expression. Moreover,
FGF-2 effect on lactotrope differentiation is mediated, at least
partially, by stimulation of the Ras-signaling pathway. Our results
suggest that, indeed, GHFT cells represent a valid model for studying
lactotropic differentiation and that FGF-2 could play a key role both
in initiating lactotrope differentiation and maintaining
PRL expression.
Differentiation of Lactotrope Precursor GHFT Cells in
Response to Fibroblast Growth Factor-2*
§¶
,
Department of Pharmacology and Center for
Molecular Genetics, University of California, San Diego, La Jolla,
California 92093-0636, § Instituto de Investigaciones
Biomédicas "Alberto Sols," Consejo Superior de
Investigaciones Científicas and Universidad Autónoma,
Madrid 28029, Spain, and ¶ Unidad de Endocrinología e
Instituto de Investigación, Fundación Hospital
Alcorcón, 29022 Alcorcón, Spain
*
This work was supported in part by National Institutes of
Health Grant DK 38524, by Dirección General de Ense
anza
Superior e Investigación Científica Grant PM97-0135, by
Grant 08.1/0032/1998 from the Comunidad de Madrid, and by the
"Fundación Salud 2000" (Serono).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Supported by Fondo de Investigaciones Sanitarias Grant FIS/BAE
93/5523 and Ministerio de Educación y Ciencia Grant 42060493EX95. Present address: Servicio de Endocrinología y Nutrición,
Hospital Universitario de Canarias, 38320 Santa Cruz de Tenerife, Spain.
**
To whom correspondence should be addressed: Inst. de
Investigaciones Biomédicas, Consejo Superior de Investigaciones
Científicas, Arturo Duperier 4, 28029 Madrid, Spain. Tel.:
34-91-585-4642; Fax: 34-91-585-4587; E-mail: aaranda@iib.uam.es.
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