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Submitted on September 15, 2005
Accepted on October 31, 2005
Prince Henry's Institute of Medical Research, P.O. BOX 5152, Clayton, VIC 3168, Australia; Monash University Department of Obstetrics & Gynaecology, Clayton, VIC 3168, Australia
* To whom correspondence should be addressed. E-mail: Lois.Salamonsen{at}princehenrys.org.
Embryo implantation and trophoblast invasion are tightly regulated processes, involving sophisticated communication between maternal decidual and fetal trophoblast cells. Decidualization is a prerequisite for successful implantation and is promoted by a number of paracrine agents, including activin A. To understand the downstream mechanisms of activin-promoted decidualization, the effects of activin on matrix metalloproteinases (MMPs) (important mediators of decidualization) were investigated. Activin A stimulated endometrial production of proMMPs-2, -3, -7, -9 and active MMP-2. In contrast, inhibin A was a potent inhibitor of proMMP-2, and antagonized the effect of activin on MMPs. Activin is upregulated with decidualization, and MMPs-2, -3 and -9 increase in parallel. Further, proMMP-2 production is stimulated when decidualization is accelerated with activin, and suppressed when activin is neutralized, attenuating decidualization. These data support that activin A promotes decidualization through upregulating MMPs. Previous in vitro evidence proposes further roles for activin and MMPs in promoting trophoblast invasion, therefore we examined their inter-relationships in early human implantation sites. MMPs-7 and -9 were produced by static cytotrophoblast subpopulations, while MMP-2 was strikingly upregulated in invasive extravillous cytotrophoblasts (EVT). Maternal decidua is the primary source of activin, where a role in stimulating MMP-2 in iEVTs can be envisaged. Inhibin was absent from cytotrophoblast populations, except for a dramatic up-regulation in endovascular EVT plugs, coinciding with a downregulation of MMP-2. This suggests inhibin may have a role in the cessation of vascular invasion. These data support that activin, via effects on MMPs, is an important factor in the maternal-fetal dialogue regulating implantation.
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