@article{3098059,
    title = "Corticotropin-releasing hormone modulates human trophoblast invasion
through carcinoembryonic antigen-related cell adhesion molecule-1
regulation",
    author = "Bamberger, AM and Minas, V and Kalantaridou, SN and Radde, J and and Sadeghian, H and Loning, T and Charalampopoulos, L and Brummer, J and and Wagener, C and Bamberger, CM and Schulte, HM and Chrousos, GP and and Makrigiannakis, A",
    journal = "American Journal of Pathology",
    year = "2006",
    volume = "168",
    number = "1",
    pages = "141-150",
    publisher = "EXCERPTA MEDICA INC-ELSEVIER SCIENCE INC",
    issn = "0002-9440",
    doi = "10.2353/ajpath.2006.050167",
    abstract = "Abnormalities in the process of trophoblast invasion may result in
abnormal placentation. Both the embryonic trophoblast and maternal
decidua produce corticotropin-releasing hormone (CRH), which promotes
implantation. Carcinoembryonic antigen-related cell adhesion molecule 1
(CEACAM1), which is expressed in extravillous trophoblasts (EVTs) of
normal human placenta, may also function in trophoblast/endometrial
interactions. We investigated whether locally produced CRH plays a role
in trophoblast invasion, primarily by regulating CEACAM1 expression. We
examined cultures of freshly isolated human EVTs, which express CEACAM1,
and an EVT-based hybridoma cell line, which is devoid of endogenous
CEACAM1. CRH inhibited EVT invasion in Matrigel invasion assays, and
this effect was blocked by the CRH receptor type 1 (CRHR1)-specific
antagonist antalarmin. Additionally, CRH decreased CEACAM1 expression in
EVTs in a dose-dependent manner. After transfection of the hybridoma
cell line with a CEACAM1 expression vector, the invasiveness of these
cells was strongly enhanced. This effect was inhibited by addition of
blocking monoclonal antibody against CEACAM1. Furthermore, blocking of
endogenous CEACAM1 in EVTs inhibited the invasive potential of these
cells. Taken together these findings suggest that CRH inhibits
trophoblast invasion by decreasing the expression of CEACAM1 through
CRHR1, an effect that might be involved in the pathophysiology of
clinical conditions, such as preeclampsia and placenta accreta."
}