In:
American Journal of Physiology-Endocrinology and Metabolism, American Physiological Society, Vol. 305, No. 1 ( 2013-07-01), p. E41-E49
Abstract:
In the present work, we investigated the effect of 17β-estradiol (E 2 ) and basic fibroblast growth factor 2 (FGF2) on the lactotroph cell-proliferative response and the related membrane-initiated signaling pathway. Anterior pituitary mixed-cell cultures of random, cycling 3-mo-old female rats were treated with 10 nM E 2 , E 2 membrane-impermeable conjugated BSA (E 2 -BSA), PPT (ERα agonist), and DPN (ERβ agonist) alone or combined with FGF2 (10 ng/ml) for 30 min or 4 h. Although our results showed that the uptake of BrdU into the nucleus of lactotrophs was not modified by E 2 or FGF2 alone, a significant increase in the lactotroph uptake of BrdU was observed after E 2 /FGF2 coincubation, with this effect being mimicked by PPT/FGF2. These proliferative effects were blocked by ICI 182,780 or PD-98059. The involvement of membrane ER in the proliferative response of prolactin cells induced by the steroid and FGF2 coincubation was confirmed using E 2 -BSA, and the association between ERα and FGF receptor was observed after E 2 /FGF2 treatment by immunoprecipitation. A significant increase in the ERK1/2 expression was noted after E 2 , E 2 -BSA, PPT, and FGF2 alone, which was more noticeable after E 2 -BSA/FGF2, E 2 /FGF2, or PPT/FGF2 treatments. This study provides evidence that E 2 and FGF2 exert a cooperative effect on the lactotroph proliferation principally by signaling initiated at the plasma membrane triggering a genomic effect mediated by MEK/ERK1/2, a common signaling pathway, that finally regulates the lactotroph population, thus contributing to pituitary plasticity.
Type of Medium:
Online Resource
ISSN:
0193-1849
,
1522-1555
DOI:
10.1152/ajpendo.00027.2013
Language:
English
Publisher:
American Physiological Society
Publication Date:
2013
detail.hit.zdb_id:
1477331-4
SSG:
12
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