Skip Navigation



Hum. Reprod. Advance Access published online on September 9, 2005

Human Reproduction, doi:10.1093/humrep/dei296
This Article
Right arrow FREE Full Text (PDF ) Freely available
Right arrow All Versions of this Article:
21/1/303    most recent
dei296v1
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Liu, Y.M.
Right arrow Articles by Yip, S.K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Liu, Y.M.
Right arrow Articles by Yip, S.K.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2005. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved.
Received June 6, 2005
Revised August 10, 2005
Accepted August 12, 2005

Article

17{beta}-Estradiol suppresses proliferation of fibroblasts derived from cardinal ligaments in patients with or without pelvic organ prolapse

Y.M. Liu 1, K.W. Choy 1, W.T. Lui 1, M.W. Pang 1, Y.F. Wong 1, and S.K. Yip 1*

1 Department of Obstetrics and Gynaecology, The Chinese University of Hong Kong, Prince of Wales Hospital, Shatin, New Territories, Hong Kong

* To whom correspondence should be addressed.
S.K. Yip, E-mail: yipsk{at}cuhk.edu.hk


   Abstract

BACKGROUND: Estrogen replacement therapy (ERT) has been used in the treatment of pelvic organ prolapse (POP) but clinical results are inconclusive. The purpose of this study was to investigate the effect of 17{beta}-estradiol (E2) on the proliferation of fibroblasts derived from cardinal ligaments in women with or without POP. METHODS: Fibroblasts were derived from seven patients with POP and seven age-matched controls. The growth rate of POP fibroblasts was compared with that of control by 3-(4,5,-dimethyl thiazolyl-2)-2,5-diphenyl tetrazolium bromide (MTT) assay. Four cell strains from each patient and control group were treated with different concentrations of E2 (10-4, 10-8, 10-9 and 10-10 mol/l). The effect of E2 on cell proliferation was then measured by MTT assay. RESULTS: The overall growth rate of POP fibroblasts was significantly slower than that of controls under normal culture conditions. Addition of E2 suppressed cell proliferation of all the fibroblasts, especially in POP fibroblasts. POP fibroblasts showed a significantly lower proliferative rate than that of controls at all E2 concentrations, with the most prominent inhibitory effect at physiological concentration (10.83 ± 34.41% versus 81.56 ± 48.10% at 10-8 mol/l). CONCLUSIONS: Our results suggest that decreased fibroblast turnover may contribute to the development of POP; and ERT may not be an effective POP treatment.

Keywords: 17{beta}-estradiol/cardinal ligament/cell proliferation/fibroblasts/pelvic organ prolapse.
Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
Hum ReprodHome page
L.W.C. Ng, S.K. Yip, H.K. Wong, G. H. Yam, Y.M. Liu, W.T. Lui, C.C. Wang, and K.W. Choy
Adipose-derived stem cells from pregnant women show higher proliferation rate unrelated to estrogen
Hum. Reprod., May 1, 2009; 24(5): 1164 - 1170.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.