Home  |  Archive  |  Online Submission  |  News & Events  |  Subscribe  |  APFA  |  Society  |  Links  |  Contact Us  |  中文版
Search   
 
Journal

Ahead of print
Authors' Accepted
    Manuscripts
new!
Current Issue
Archive
Acknowledgments
Special Issues
Browse by Category

Manuscript Submission

Online Submission
Online Review
Instruction for Authors
Instruction for Reviewers
English Corner new!

About AJA

About AJA
Editorial Board
Contact Us
News

Resources & Services

Advertisement
Subscription
Email alert
Proceedings
Reprints

Download area

Copyright licence
EndNote style file
Manuscript word template
Guidance for AJA figures
    preparation (in English)

Guidance for AJA figures
    preparation (in Chinese)

Proof-reading for the
    authors

AJA Club (in English)
AJA Club (in Chinese)

Links

Meetings
Journals
Societies & Institutes
Hospitals
Databases & Libraries
Companies
Websites
Other links

 
Abstract

Volume 14, Issue 4 (July 2012) 14, 546–555; 10.1038/aja.2011.181

Reduced prostate branching morphogenesis in stromal fibroblast, but not in epithelial, estrogen receptor α knockout mice

Ming Chen, Chiuan-Ren Yeh, Chih-Rong Shyr, Hsiu-Hsia Lin, Jun Da and Shuyuan Yeh

Departments of Urology and Pathology, University of Rochester Medical Center, Rochester, NY 14642, USA.

Correspondence: Dr SY Yeh (shuyuan_yeh@urmc.rochester.edu)

Received: 27 April 2011; Revised: 12 September 2011; Accepted: 2 December 2011; Published online: 21 May 2012

Abstract

Early studies suggested that estrogen receptor alpha (ERa) is involved in estrogen-mediated imprinting effects in prostate
development. We recently reported a more complete ERa knockout (KO) mouse model via mating b-actin Cre transgenic mice with floxed ERa mice. These ACTB-ERaKO male mice showed defects in prostatic branching morphogenesis, which demonstrates that ERa is necessary to maintain proliferative events in the prostate. However, within which prostate cell type ERa exerts those important functions remains to be elucidated. To address this, we have bred floxed ERa mice with either fibroblast-specific protein (FSP)-Cre or probasin-Cre transgenic mice to generate a mouse model that has deleted ERa gene in either stromal fibroblast (FSP-ERaKO) or pithelial (pes-ERaKO) prostate cells. We found that circulating testosterone and fertility were not altered in FSP-ERaKO and pes-ERaKO male mice. Prostates of FSP-ERaKO mice have less branching morphogenesis compared to that of wild-type littermates. Further analyses indicated that loss of stromal ERa leads to increased stromal apoptosis, reduced expression of insulin-like growth factor-1 (IGF-1) and FGF10, and increased expression of BMP4. Collectively, we have established the first in vivo prostate stromal and epithelial selective ERaKOmouse models and the results from these mice indicated that stromal fibroblast ERa plays important roles in prostatic branching morphogenesis via a paracrine fashion. Selective deletion of the ERa gene in mouse prostate epithelial cells by probasin-Cre does not affect the regular prostate development and homeostasis.

Keywords: Cre-loxP; estrogen receptor; knockout; prostate; stromal–epithelial interaction

PDF | 中文摘要 |

 
Browse:  2171
 
Copyright 1999-2017  Shanghai Materia Medica, Shanghai Jiao Tong University.  All rights reserved