Syndecan-1 does not regulate the expression of CXCL1 through the MAPK signalling pathway in decidualized human endometrial stromal cells

Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: SUN 554-573-Ovarian & Uterine Function I
Sunday, June 16, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board SUN-570
Alexandra Petra Hess*1, Olga Altergot-Ahmad2, Sarah Jean Böddeker2, Jan Steffen Krüssel2 and Dunja Maria Baston-Büst2
1University Düsseldorf Medical Center, Düsseldorf, Germany, 2University Düsseldorf Medical Center
Syndecan-1 does not regulate the expression of CXCL1 through the MAPK signalling pathway in decidualized human endometrial stromal cells

O. Altergot-Ahmad§, A.P. Hess§, S.J. Böddeker, J.-S. Krüssel, D.M. Baston-Büst

§ shared 1st authorship

University Düsseldorf, Medical Faculty, Department of OB/GYN and REI (UniKiD), Moorenstr. 5, 40225 Düsseldorf, Germany  



Background: A successful implantation of the embryo in the human endometrium is essential for a subsequent proper pregnancy. This highly sensitive process involves a variety of cytokines like chemokines, growth factors and different modulating factors. C-X-C-motiv ligand 1 (CXCL1), one of the most important chemokines during implantation, mediates its function through a G-protein coupled receptor second messenger cascade by the CXC-receptor 2 (CXCR2) and the co-receptor Syndecan-1 (Sdc-1). Previous studies of Sdc-1 by use of the knock down cell line KdS1 offered changes in cytokine and angiogenic factor expression of decidualized KdS1 after incubation with embryonic stimuli. This study is concerned with different signalling pathways controlling the expression of CXCL1 in the Sdc1-1 knock down cell line KdS1.

Methods: The immortalized human endometrial stromal cell line St-T1 was transfected with Sdc-1 shRNA. The inducible stable Sdc-1 knock-down cell line generated was named KdS1. After incubation with mitogen-activated protein kinase kinase (MEK) inhibitor, signal transducer and activator of transcription (STAT) inhibitor and c-Jun N-terminal kinases (JNK) inhibitor for 2h and subpurchaser incubation with the embryo surrogate marker IL-1β for 48h, CXCL1 ELISA was performed. Experiments were carried out with decidualized (d) St-T1 and KdS1 cells where the decidualization was proven on the mRNA level by amplification of prolactin by PCR. Statistical analyses were performed by applying the Student's t-test with p < 0.05.

Results: The incubation of dSt-T1 and dKdS1 cells with the MEK inhibitor revealed a significant decrease in the expression of CXCL1. In both cell lines, the CXCL1 expression decreased to 40%. The inhibition of JNK and STAT showed no effect on CXCL1 expression.

Conclusion: MAPK pathway containing MEK mediates a variety of processes during embryonic implantation. The expression of CXCL1 in human decidua in vitro is mediated via MAPK pathway independent from presence or absence of Sdc-1, which is already known to regulate cell-cycle pathways via MAPK.

Nothing to Disclose: APH, OA, SJB, JSK, DMB

*Please take note of The Endocrine Society's News Embargo Policy at

Sources of Research Support: German Research Foundation (DFG) to AP Hess (HE 3544/2-2)