Skip Navigation



Hum. Reprod. Advance Access published online on July 31, 2006

Human Reproduction, doi:10.1093/humrep/del297
This Article
Right arrow FREE Full Text (PDF ) Freely available
Right arrow All Versions of this Article:
21/12/3059    most recent
del297v1
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 Collette, T.
Right arrow Articles by Akoum, A.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Collette, T.
Right arrow Articles by Akoum, A.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2006. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Received February 2, 2006
Revised June 13, 2006
Accepted June 23, 2006

Article

Increased expression of matrix metalloproteinase-9 in the eutopic endometrial tissue of women with endometriosis

T. Collette 1, R. Maheux 2, J. Mailloux 3, and A. Akoum 2 *

1 Centre de Recherche, Hôpital Saint-François d’Assise, Centre Hospitalier Universitaire de Québec, Canada
2 Centre de Recherche, Hôpital Saint-François d’Assise, Centre Hospitalier Universitaire de Québec; Département d’Obstétrique et Gynécologie, Faculté de Médecine, Université Laval, Québec, Canada
3 Département d’Obstétrique et Gynécologie, Faculté de Médecine, Université Laval, Québec, Canada

* To whom correspondence should be addressed.
A. Akoum, E-mail: ali.akoum{at}crsfa.ulaval.ca


   Abstract

BACKGROUND: Endometriosis is a disease where endometrial tissue implants in ectopic locations. Remodelling of the extracellular matrix (ECM) is a prerequisite for the implantation of this tissue to be possible. METHODS: In this study, we detected immunoreactive matrix metalloproteinase-9 (MMP-9) throughout endometrial tissue and identified von Willebrand factor (vWF)-positive endothelial cells, CD45-positive leukocytes, CD3-positive T lymphocytes and CD68-positive macrophages as cells expressing MMP-9 in the stroma. RESULTS: We found an increased expression of MMP-9 in the uterine endometrial tissue of women with endometriosis, as assessed by zymography and enzyme-linked immunosorbent assay (ELISA) (P < 0.05). However, RT-PCR did not show a statistically significant increase in MMP-9 mRNA expression in these tissues (P = 0.14). There was no significant difference between women with and without endometriosis in the expression of tissue inhibitor of MMPs (TIMP)-1, a known natural inhibitor of the pro- and active forms of MMP-9, whether tested by ELISA or by RT-PCR (P = 0.46 and 0.37, respectively). Interestingly, the ratio of MMP-9/TIMP-1 expression was significantly higher in women with endometriosis than in normal women both at the protein and the mRNA levels (P < 0.05). CONCLUSION: These findings make plausible the involvement of MMP-9/TIMP-1 imbalance in the invasiveness of the endometrial tissue of patients with endometriosis and the ectopic development of the disease.

Keywords: endometriosis/endometrium/matrix metalloproteinase-9/tissue inhibitor of matrix metalloproteinase.
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
ReproductionHome page
M Pino, C Galleguillos, M Torres, H Sovino, A Fuentes, M A Boric, and M C Johnson
Association between MMP1 and MMP9 activities and ICAM1 cleavage induced by tumor necrosis factor in stromal cell cultures from eutopic endometria of women with endometriosis
Reproduction, November 1, 2009; 138(5): 837 - 847.
[Abstract] [Full Text] [PDF]


Home page
Reproductive SciencesHome page
M. Pitsos and N. Kanakas
The Role of Matrix Metalloproteinases in the Pathogenesis of Endometriosis
Reproductive Sciences, August 1, 2009; 16(8): 717 - 726.
[Abstract] [PDF]


Home page
Hum ReprodHome page
P. Akkaya, G. Onalan, N. Haberal, N. Bayraktar, B. Mulayim, and H. B. Zeyneloglu
Doxycycline causes regression of endometriotic implants: a rat model
Hum. Reprod., August 1, 2009; 24(8): 1900 - 1908.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Pathol.Home page
P. D'Amora, T. T. Maciel, R. Tambellini, M. A. Mori, J. B. Pesquero, H. Sato, M. J. B. C. Girao, I. D. C. Guerreiro da Silva, and E. Schor
Disrupted Cell Cycle Control in Cultured Endometrial Cells from Patients with Endometriosis Harboring the Progesterone Receptor Polymorphism PROGINS
Am. J. Pathol., July 1, 2009; 175(1): 215 - 224.
[Abstract] [Full Text] [PDF]


Home page
Hum ReprodHome page
J. Yu, Y. Wang, W.-H. Zhou, L. Wang, Y.-Y. He, and D.-J. Li
Combination of estrogen and dioxin is involved in the pathogenesis of endometriosis by promoting chemokine secretion and invasion of endometrial stromal cells
Hum. Reprod., July 1, 2008; 23(7): 1614 - 1626.
[Abstract] [Full Text] [PDF]


Home page
Mol Hum ReprodHome page
M.C. Ferreira, C.A. Witz, L.S. Hammes, N. Kirma, F. Petraglia, R.S. Schenken, and F.M. Reis
Activin A increases invasiveness of endometrial cells in an in vitro model of human peritoneum
Mol. Hum. Reprod., May 1, 2008; 14(5): 301 - 307.
[Abstract] [Full Text] [PDF]


Home page
ReproductionHome page
S Guay and A Akoum
Stable inhibition of interleukin 1 receptor type II in Ishikawa cells augments secretion of matrix metalloproteinases: possible role in endometriosis pathophysiology
Reproduction, September 1, 2007; 134(3): 525 - 534.
[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.