Document Detail

Estradiol partially recapitulates murine pituitary cell cycle response to pregnancy.
MedLine Citation:
PMID:  22851678     Owner:  NLM     Status:  MEDLINE    
Because pregnancy and estrogens both induce pituitary lactotroph hyperplasia, we assessed the expression of pituitary cell cycle regulators in two models of murine pituitary hyperplasia. Female mice were assessed during nonpregnancy, pregnancy, day of delivery, and postpartum. We also implanted estradiol (E(2)) pellets in female mice and studied them for 2.5 months. Pituitary weight in female mice increased 2-fold after E(2) administration and 1.4-fold at day of delivery, compared with placebo-treated or nonpregnant females. Pituitary proliferation, as assessed by proliferating cell nuclear antigen and/or Ki-67 staining, increased dramatically during both mid-late pregnancy and E(2) administration, and lactotroph hyperplasia was also observed. Pregnancy induced pituitary cell cycle proliferative and inhibitory responses at the G(1)/S checkpoint. Differential cell cycle regulator expression included cyclin-dependent kinase inhibitors, p21(Cip1), p27(Kip1), and cyclin D1. Pituitary cell cycle responses to E(2) administration partially recapitulated those effects observed at mid-late pregnancy, coincident with elevated circulating mouse E(2), including increased expression of proliferating cell nuclear antigen, Ki-67, p15(INK4b), and p21(Cip1). Nuclear localization of pituitary p21(Cip1) was demonstrated at mid-late pregnancy but not during E(2) administration, suggesting a cell cycle inhibitory role for p21(Cip1) in pregnancy, yet a possible proproliferative role during E(2) administration. Most observed cell cycle protein alterations were reversed postpartum. Murine pituitary meets the demand for prolactin during lactation associated with induction of both cell proliferative and inhibitory pathways, mediated, at least partially, by estradiol.
Yoel Toledano; Svetlana Zonis; Song-Guang Ren; Kolja Wawrowsky; Vera Chesnokova; Shlomo Melmed
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2012-07-31
Journal Detail:
Title:  Endocrinology     Volume:  153     ISSN:  1945-7170     ISO Abbreviation:  Endocrinology     Publication Date:  2012 Oct 
Date Detail:
Created Date:  2012-09-24     Completed Date:  2012-12-11     Revised Date:  2013-10-10    
Medline Journal Info:
Nlm Unique ID:  0375040     Medline TA:  Endocrinology     Country:  United States    
Other Details:
Languages:  eng     Pagination:  5011-22     Citation Subset:  AIM; IM    
Department of Medicine, Cedars-Sinai Medical Center, Los Angeles, California 90048, USA.
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MeSH Terms
Cell Cycle / drug effects*,  genetics
Cell Division / drug effects*,  genetics
Cell Proliferation / drug effects*
Cyclin D1 / genetics,  metabolism
Cyclin-Dependent Kinase Inhibitor p21 / genetics,  metabolism
Estradiol / pharmacology*
Ki-67 Antigen / genetics,  metabolism
Pituitary Gland / drug effects*,  metabolism
Pregnancy, Animal
Grant Support
Reg. No./Substance:
0/Cyclin-Dependent Kinase Inhibitor p21; 0/Ki-67 Antigen; 136601-57-5/Cyclin D1; 50-28-2/Estradiol

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