Skip Navigation

This Article
Right arrow FREE Full Text (PDF ) Freely available
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 ISI Web of Science
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 arrow Search for citing articles in:
ISI Web of Science (51)
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by McLaren, J.
Right arrow Articles by Smith, S. K.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McLaren, J.
Right arrow Articles by Smith, S. K.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Human Reproduction, Vol 12, 146-152, Copyright © 1997 by Oxford University Press

ARTICLES

Immunolocalization of the apoptosis regulating proteins Bcl-2 and Bax in human endometrium and isolated peritoneal fluid macrophages in endometriosis

J McLaren, A Prentice, DS Charnock-Jones, AM Sharkey and SK Smith
Department of Obstetrics and Gynaecology, University of Cambridge, Rosie Maternity Hospital, UK.

Endometriosis, a debilitating disease associated with infertility, is characterized by the prolonged presence of ectopic endometrial tissue and the involvement of activated peritoneal fluid macrophages. Apoptosis, which occurs in both endometrium and peritoneal fluid macrophages, is controlled in part by members of the Bcl-2/Bax family of proteins. Here, through immunohistochemical staining, we investigated the Bcl-2/Bax status in endometrium and peritoneal fluid macrophages in endometriosis. Bcl-2/Bax immunoreactivity was found predominantly in the glandular epithelial cells, mainly during the proliferative phase of the menstrual cycle for Bcl-2 but throughout the entire menstrual cycle for Bax. Ectopic endometrium contained a population of Bcl-2 positive. Bax negative tissue macrophages. Fluorescence-activated cell sorting of isolated peritoneal fluid macrophages showed that women with endometriosis had a significantly higher proportion of Bcl-2 positive macrophages than the non- endometriotic group. The proportion of Bax positive peritoneal fluid macrophages was significantly elevated in women without endometriosis. The increased proportion of Bcl-2 positive macrophages found in women with endometriosis may predispose these cells to resist apoptosis. The continued survival of these active cells could have important consequences for the survival and proliferation of the ectopic endometrial tissue.
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
K. N. Khan, H. Masuzaki, A. Fujishita, M. Kitajima, K. Hiraki, I. Sekine, T. Matsuyama, and T. Ishimaru
Interleukin-6- and tumour necrosis factor {alpha}-mediated expression of hepatocyte growth factor by stromal cells and its involvement in the growth of endometriosis
Hum. Reprod., October 1, 2005; 20(10): 2715 - 2723.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
W. Chien, T. Kumagai, C. W. Miller, J. C. Desmond, J. M. Frank, J. W. Said, and H. P. Koeffler
Cyr61 Suppresses Growth of Human Endometrial Cancer Cells
J. Biol. Chem., December 17, 2004; 279(51): 53087 - 53096.
[Abstract] [Full Text] [PDF]

Home page
 Hum Reprod UpdateHome page
T. Harada, A. Kaponis, T. Iwabe, F. Taniguchi, G. Makrydimas, N. Sofikitis, M. Paschopoulos, E. Paraskevaidis, and N. Terakawa
Apoptosis in human endometrium and endometriosis
Hum. Reprod. Update, January 1, 2004; 10(1): 29 - 38.
[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.