PMID- 25653281
OWN - NLM
STAT- MEDLINE
DCOM- 20160222
LR  - 20150327
IS  - 1529-7268 (Electronic)
IS  - 0006-3363 (Linking)
VI  - 92
IP  - 3
DP  - 2015 Mar
TI  - Neonatal uterine and vaginal cell proliferation and adenogenesis are independent 
      of estrogen receptor 1 (ESR1) in the mouse.
PG  - 78
LID - 10.1095/biolreprod.114.125724 [doi]
AB  - Neonatal uterus and vagina express estrogen receptor 1 (ESR1) and respond 
      mitogenically to exogenous estrogens. However, neonatal ovariectomy does not 
      inhibit preweaning uterine cell proliferation, indicating that this process is 
      estrogen independent. Extensive literature suggests that ESR1 can be activated by 
      growth factors in a ligand-independent manner and drive uterine cell 
      proliferation. Alternatively, neonatal uterine cell proliferation could be ESR1 
      independent despite its obligatory role in adult luminal epithelial 
      proliferation. To determine ESR1's role in uterine and vaginal development, we 
      analyzed cell proliferation, apoptosis, and uterine gland development 
      (adenogenesis) in wild-type (WT) and Esr1 knockout (Esr1KO) mice from Postnatal 
      Day 2 to Postnatal Day 60. Uterine and vaginal cell proliferation, apoptosis, and 
      uterine adenogenesis were comparable in WT and Esr1KO mice before weaning. By 
      Days 29-60, glands had regressed, and uterine cell proliferation was reduced in 
      Esr1KO mice in contrast to continued adenogenesis and proliferation in WT. 
      Apoptosis in Esr1KO uterine epithelium was not increased compared to WT at any 
      age, indicating that differences in cell proliferation, rather than apoptosis, 
      cause divergence of uterine size in these two groups at puberty. Similarly, 
      vaginal epithelial proliferation was reduced, and the epithelium became atrophic 
      in Esr1KO mice by 29 days of age and later in Esr1KO mice. These results indicate 
      that preweaning uterine and vaginal development is ESR1 independent but becomes 
      dependent on ESR1 by Day 29 on. It is not yet clear what mechanisms drive 
      preweaning vaginal and uterine development, but ligand-independent activation of 
      ESR1 is not involved.
CI  - (c) 2015 by the Society for the Study of Reproduction, Inc.
FAU - Nanjappa, Manjunatha K
AU  - Nanjappa MK
AD  - Department of Physiological Sciences, College of Veterinary Medicine, University 
      of Florida, Gainesville, Florida.
FAU - Medrano, Theresa I
AU  - Medrano TI
AD  - Department of Physiological Sciences, College of Veterinary Medicine, University 
      of Florida, Gainesville, Florida.
FAU - March, Amelia G
AU  - March AG
AD  - Department of Physiological Sciences, College of Veterinary Medicine, University 
      of Florida, Gainesville, Florida.
FAU - Cooke, Paul S
AU  - Cooke PS
AD  - Department of Physiological Sciences, College of Veterinary Medicine, University 
      of Florida, Gainesville, Florida paulscooke@ufl.edu.
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20150204
PL  - United States
TA  - Biol Reprod
JT  - Biology of reproduction
JID - 0207224
RN  - 0 (Estrogen Receptor alpha)
RN  - 4G7DS2Q64Y (Progesterone)
SB  - IM
MH  - Animals
MH  - Animals, Newborn/*physiology
MH  - Apoptosis/physiology
MH  - Cell Proliferation/*physiology
MH  - Epithelial Cells/cytology/physiology
MH  - Estrogen Receptor alpha/deficiency/genetics/*physiology
MH  - Female
MH  - Genotype
MH  - Heterozygote
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Mice, Knockout
MH  - Models, Animal
MH  - Progesterone/physiology
MH  - Sexual Maturation/genetics/physiology
MH  - Time Factors
MH  - Uterus/*cytology/*growth & development/physiology
MH  - Vagina/*cytology/*growth & development/physiology
OTO - NOTNLM
OT  - 17beta-estradiol
OT  - progesterone
OT  - uterine glands
EDAT- 2015/02/06 06:00
MHDA- 2016/02/24 06:00
CRDT- 2015/02/06 06:00
PHST- 2015/02/06 06:00 [entrez]
PHST- 2015/02/06 06:00 [pubmed]
PHST- 2016/02/24 06:00 [medline]
AID - biolreprod.114.125724 [pii]
AID - 10.1095/biolreprod.114.125724 [doi]
PST - ppublish
SO  - Biol Reprod. 2015 Mar;92(3):78. doi: 10.1095/biolreprod.114.125724. Epub 2015 Feb 
      4.