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Hum. Reprod. Advance Access published online on July 16, 2008
Human Reproduction, doi:10.1093/humrep/den264
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© The Author 2008. 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
The online version of this article has been published under an open access model. Users are entitled to use, reproduce, disseminate, or display the open access version of this article for non-commercial purposes provided that: the original authorship is properly and fully attributed: the Journal and Oxford University Press are attributed as the original place of publication with the correct citation details given: if an article is subsequently reproduced or disseminated not in its entirety but only in part or as a derivative word this must be clearly indicated. For commercial re-use, please contact journals.permissions@oxfordjournals.org

Regulation of MMP-9 by p53 in first trimester cytotrophoblastic cells

M. Cohen1, C. Wuillemin, O. Irion and P. Bischof

Department of Obstetrics and Gynaecology, Maternity, Laboratory of Hormonology, University of Geneva, 30 Boulevard de la Cluse, 1211, Geneva 14, Switzerland

1 Correspondence address. Tel: +41-22-38-24-381; Fax: +41-22-38-24-310; E-mail: marie.cohen{at}hcuge.ch

BACKGROUND: The matrix metalloproteinase (MMP) family is known to play a key role in tissue remodelling during embryonic development and in pathological conditions, such as cardiovascular disease, arthritis and cancer metastasis. It has been shown previously that p53 regulates positively or negatively the expression of different MMPs. Because of p53 overexpression in trophoblastic cells, and its potential role in regulating MMP-2 and MMP-9 expression in different cell lines, we hypothesized that the expression of MMP-9 could also be regulated by p53 in first trimester cytotrophoblasts (CTB).

METHODS and RESULTS: Transfection experiments in CTB demonstrated that wild-type p53 down-regulates the –670 (P < 0.001) but not the –531 and –90 human MMP-9 promoter/CAT reporter plasmid activity, whereas p53 mutants partially lost this repressive activity. However, endogenous p53 is not able to regulate MMP-9 expression in CTB. The presence of high molecular weight complexes of p53 in CTB suggests a potential mechanism of inactivation of p53 transcriptional activity towards MMPs in these cells.

CONCLUSIONS: Although p53 is mutated in trophoblast, it is functionally incompetent towards MMPs in these cells.

Key words: matrix metalloproteinase-2/matrix metalloproteinase-9/p53/first trimester cytotrophoblast/gelatinase

Submitted on February 26, 2008; resubmitted on May 9, 2008; accepted on June 9, 2008.


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