Osteopontin Is Colocalized with the Adhesion Molecule CEACAM1 in the Extravillous Trophoblast of the Human Placenta and Enhances Invasion of CEACAM1-Expressing Placental Cells

Briese, Juliane; Oberndörfer, Marine; Pätschenik, Christine; Schulte, Heinrich M.; Makrigiannakis, Antonis; Löning, Thomas; Bamberger, Ana‐Maria

doi:10.1210/jc.2004-2434

Cited by 37 publications

(20 citation statements)

References 34 publications

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“…Plasmid DNA for transfection was prepared using the QIAGEN Maxi Kit (QIAGEN, Mississauga, Canada). WRO cells which did not endogenously express CEACAM1 were selected for stable forced expression of CEACAM1-L using the pcDNA 3.1(À)/Zeo-L-CEACAM1 expression vector as described previously (Briese et al, 2005). Empty vector served as a control.…”

Section: Ceacam1 Silencing or Overexpression In Human Thyroid Carcinomentioning

confidence: 99%

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

Winer

et al. 2006

Oncogene

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Section: Ceacam1 Silencing or Overexpression In Human Thyroid Carcinomentioning

confidence: 99%

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

Winer

et al. 2006

Oncogene

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“…The extravillous trophoblasts of the human placenta also express OPN, which regulates the invasiveness of these cells (12). Gabinskaya et al studied human placentas with immunostaining.…”

Section: Discussionmentioning

confidence: 99%

“…It is involved in adhesion and signal transduction at the uterine-placental interface (11). OPN has also been found in the trophoblast of the human placenta, and it can enhance the invasiveness of trophoblast cells in vitro (12). Furthermore, OPN is expressed by endothelial, vascular smooth muscle cells (VSMCs) and immune cells (13,14), and it acts as a proinflammatory Th1 type cytokine (15).…”

Section: Introductionmentioning

confidence: 99%

Plasma osteopontin concentrations in preeclampsia – is there an association with endothelial injury?

Stenczer

Rigó

Prohászka

et al. 2009

Clinical Chemistry and Laboratory Medicine

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Background: It has been previously reported that plasma osteopontin (OPN) concentrations are increased in cardiovascular disorders. The goal of the present study was to determine plasma OPN concentrations in healthy pregnant women and preeclamptic patients, and to investigate their relationship to the clinical characteristics of the study subjects and to markers of inflammation wC-reactive protein (CRP)x, endothelial activation wvon Willebrand factor antigen (VWF:Ag)x or endothelial injury (fibronectin), oxidative stress wmalondialdehyde (MDA)x and trophoblast debris (cellfree fetal DNA). Methods: Forty-four patients with preeclampsia and 44 healthy pregnant women matched for age and gestational age were involved in this case-control study. Plasma OPN concentrations were measured with ELISA. Serum CRP concentrations were determined with an autoanalyzer using the manufacturer's reagents. Plasma VWF:Ag was quantified by ELISA, while plasma fibronectin concentrations were measured by nephelometry. Plasma MDA concentrations were estimated by the thiobarbituric acid-based colorimetric assay. The amount of cell-free fetal DNA in maternal plasma was determined by quantitative real-time PCR analysis of the sexdetermining region Y (SRY) gene. For statistical analyses, non-parametric methods were applied.

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“…40,47 Recently, osteopontin, a secreted ECM glycoprotein, and CEACAM1 were suggested to act as a functional complex to enhance invasiveness of trophoblast cells. 48 Thus, CEACAM1 is able to interact and interfere with integrins or integrin-regulated cellular functions and therefore to affect the cellular interactions with the ECM.…”

Section: Discussionmentioning

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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Osteopontin Is Colocalized with the Adhesion Molecule CEACAM1 in the Extravillous Trophoblast of the Human Placenta and Enhances Invasion of CEACAM1-Expressing Placental Cells

Cited by 37 publications

References 34 publications

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

CEACAM1 impedes thyroid cancer growth but promotes invasiveness: a putative mechanism for early metastases

Plasma osteopontin concentrations in preeclampsia – is there an association with endothelial injury?

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

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