Effects of human trophoblast-induced interferons on the expression of proto-oncogenes c-fms/CSF-1R, EGF-R and c-erbB2 in invasive and non-invasive trophoblast

Aboagye-Mathiesen, George; Zcravkovic, M.; Tóth, Ferenc; Ebbesen, Peter

doi:10.1016/s0143-4004(97)90087-4

Cited by 20 publications

(16 citation statements)

References 25 publications

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“…22 Ten placentas were obtained from healthy women after legal termination of pregnancy (5 to 10 weeks of gestation). Informed consent and institutional review board approval were obtained.…”

Section: Isolation and Characterization Of Human Invasive Evt Populatmentioning

confidence: 99%

Corticotropin-Releasing Hormone Modulates Human Trophoblast Invasion through Carcinoembryonic Antigen-Related Cell Adhesion Molecule-1 Regulation

Bamberger

Minas

Kalantaridou

et al. 2006

The American Journal of Pathology

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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 EVTbased 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. The complex developmental process of implantation involves a series of steps leading to an effective cross-talk between invasive trophoblast cells and the maternal endometrium. This dynamic process requires a precisely coordinated development of a hormonally primed adhesive endometrium and a blastocyst competent to implant. The trophoblast undergoes a number of distinct interactions with the underlying endometrial surface initiated by apposition, which involves close proximity between trophoblast and endometrial epithelium, followed by attachment, and concluded by invasion of trophoblast into the decidualized stroma.1 However, the molecular interactions at the embryo-maternal interface during the time of adhesion and subsequent invasion are not fully understood.The hypothalamic neuropeptide corticotropin-releasing hormone (CRH) is produced in several organs of the female reproductive system, including the endometrial glands, decidualized stroma, and trophoblast. [2][3][4][5][6] In addition, the gene encoding the CRH receptor type 1Supported by the Alexander Onassis Foundation (grant to A.M. and S.N.K.) and the Deutsche Krebshilfe (grant 10-2063 to A.M.B. and J.B.).

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Section: Isolation and Characterization Of Human Invasive Evt Populatmentioning

confidence: 99%

Corticotropin-Releasing Hormone Modulates Human Trophoblast Invasion through Carcinoembryonic Antigen-Related Cell Adhesion Molecule-1 Regulation

Bamberger

Minas

Kalantaridou

et al. 2006

The American Journal of Pathology

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“…Cultures of first-trimester invasive and non-invasive trophoblast populations were established and characterized as reported previously [1]. Briefly, eight to ten placentae (5-12 weeks) obtained after legal termination of pregnancy were washed in sterile phosphate buffer saline (s-PBS), and areas rich in chorionic villi were selected and minced between scalpel blades and were subjected to three sequential 10-min treatments with 0.125 % trypsin and 0.2 mg/ml DNAse I (Boehringer Mannheim, Germany) in s-PBS containing 5 mM MgCl 2 .…”

Section: Isolation Of Invasive and Non-invasive Trophoblast Populationsmentioning

confidence: 99%

“…Their functional ability to produce hormones and the 92-kDa and 72-kDa gelatinases were described previously [1].…”

Section: Isolation Of Invasive and Non-invasive Trophoblast Populationsmentioning

confidence: 99%

Expression of the high-mobility group protein HMGI(Y) in human trophoblast: potential role in trophoblast invasion of maternal tissue

et al. 2003

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The high-mobility group protein HMGI(Y) is a member of a family of non-histone chromosomal proteins, which have been implicated in the regulation of inducible gene transcription, integration of retroviruses into chromosomes and induction of neoplastic transformation and metastatic progression in cancer cells. The human trophoblast is a tissue that shares proliferation capacity and invasiveness with neoplastic tissues, but in which these processes are tightly regulated. In the present study, we analyzed the expression of HMGI(Y) in the human placenta using immunohistochemistry. We found expression of HMGI(Y), with nuclear localization, in the villous cytotrophoblast (vCT), which is a highly proliferative cell type. In contrast, the majority of the nuclei of the villous syncytiotrophoblast, a terminally differentiated tissue, was negative. Interestingly, expression of HMGI(Y) was strongest in anchoring villi at the implantation site and in extravillous (intermediate) trophoblast (EVT) invading the maternal decidua. As vCT cells differentiate to become EVT, the HMGI(Y) protein appears to switch from a nuclear to a cytoplasmic localization. Expression of HMGI(Y) in isolated trophoblast populations in primary cell culture was also confirmed using Western-blot analysis. This study shows for the first time expression and localization of HMGI(Y) in the subpopulations of placental tissue.

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“…18 Briefly, 8 to 10 placentas (5 to 12 weeks) obtained after legal termination of pregnancy were washed in sterile phosphate-buffered saline (s-PBS) and areas rich in chorionic villi were selected and minced between scalpel blades and were subjected to three sequential 10-minute treatments with 0.125% trypsin and 0.2 mg/ml DNase I (Boehringer Mannheim, Mannheim, Germany) in s-PBS containing 5 mmol/L MgCl 2 . Cells released from each 10-minute step were pooled and filtered through two layers of muslin, resuspended in 70% Percoll (Pharmacia, Uppsala, Sweden) at a density of 2 ϫ 10 5 cells/ml, and put under 20 ml of 25% Percoll.…”

Section: Isolation Of Invasive and Noninvasive Trophoblast Populationsmentioning

confidence: 99%

“…The invasive characteristics of the extravillous trophoblast cells were determined using an in vitro Matrigel invasion assay as described 18,20 using transwells with a polycarbonate filter of 2.5-cm diameter and 8-m pore size. The upper surface of the filter was coated with Matrigel (Collaborative Research, Bedford, MA; diluted 1:20 with KGM).…”

Section: In Vitro Invasion Assaymentioning

confidence: 99%

The Adhesion Molecule CEACAM1 (CD66a, C-CAM, BGP) Is Specifically Expressed by the Extravillous Intermediate Trophoblast

Bamberger

Sudahl

Löning

et al. 2000

The American Journal of Pathology

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CEACAM1 (CD66a, C-CAM, BGP) is an adhesion molecule of the carcinoembryonic antigen family which has been shown to be normally expressed at the apical pole of epithelial cells, including the apical pole of endometrial surface and glandular epithelia. The purpose of the present study was to investigate its expression pattern at the maternal-fetal interface, and thus to determine whether CEACAM1 could be implicated in the human implantation process. For this purpose, we performed immunohistochemistry using the 4D1/C2 monoclonal antibody (mAb) as well as flow cytometry and Western blot on isolated trophoblast populations. On the maternal side of the maternalfetal interface, CEACAM1 was present in epithelial cells of pregnancy endometrium as well as in small endometrial vessels, whereas it was absent from decidual cells. On the fetal side, CEACAM1 was strongly expressed by the extravillous (intermediate) trophoblast at the implantation site, as well as by extravillous trophoblast cells with invasive phenotype in primary culture, as shown by flow cytometry and Western blot. Expression was also observed in placental villous core vessels but was absent from both villous cyto-and syncytiotrophoblasts throughout the pregnancy. We conclude that, given its specific ex- The trophoblast is the first tissue to differentiate in the mammalian conceptus and its normal development and specific properties are crucial for both implantation and further survival of the embryo. Furthermore, the placenta is unique in its ability to proliferate and invade another tissue in a controlled fashion and is thus a very interesting model for the study of molecular mechanisms involved in these processes, and for differentiating them from those implicated in tumor progression.During development of the human placenta, the stem cell-like cytotrophoblast proliferates and gives rise to the differentiated syncytiotrophoblast on the villous surface and to the invasive intermediate trophoblast, which invades the maternal tissues and provides the anchoring of the placenta and the conceptus at the maternal-fetal interface. 1 The extravillous trophoblast can be further divided into proximal extravillous trophoblast originating from the anchoring villi; deep interstitial extravillous trophoblast invading the decidual stroma and the myometrium; and endovascular trophoblast, which assumes endothelial-like characteristics. [2][3][4] Starting with the initial contact which is made between the trophoblast and the apical plasma membrane of the endometrial surface epithelial cells, through the invasion of the decidua and the invasion of decidual vessels with gradual colonization of the arterial wall of the spiral arteries, cellular contacts mediated by cell adhesion molecules are of essential importance.Cell adhesion molecules are important mediators of tissue architecture and cellular polarity which also mod-

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Effects of human trophoblast-induced interferons on the expression of proto-oncogenes c-fms/CSF-1R, EGF-R and c-erbB2 in invasive and non-invasive trophoblast

Cited by 20 publications

References 25 publications

Corticotropin-Releasing Hormone Modulates Human Trophoblast Invasion through Carcinoembryonic Antigen-Related Cell Adhesion Molecule-1 Regulation

Corticotropin-Releasing Hormone Modulates Human Trophoblast Invasion through Carcinoembryonic Antigen-Related Cell Adhesion Molecule-1 Regulation

Expression of the high-mobility group protein HMGI(Y) in human trophoblast: potential role in trophoblast invasion of maternal tissue

The Adhesion Molecule CEACAM1 (CD66a, C-CAM, BGP) Is Specifically Expressed by the Extravillous Intermediate Trophoblast

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