Skip Navigation



Hum. Reprod. Advance Access published online on August 6, 2008

Human Reproduction, doi:10.1093/humrep/den308
This Article
Right arrow Full Text
Right arrow Full Text (PDF )
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Google Scholar
Right arrow Articles by Zhou, W.-H.
Right arrow Articles by Li, D.-J.
PubMed
Right arrow PubMed Citation
Right arrow Articles by Zhou, W.-H.
Right arrow Articles by Li, D.-J.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2008. Published by Oxford University Press on behalf of the European Society of Human Reproduction and Embryology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Chemokine CXCL12 promotes the cross-talk between trophoblasts and decidual stromal cells in human first-trimester pregnancy

Wen-Hui Zhou1,2, Mei-Rong Du1,4, Lin Dong1, Jing Yu1 and Da-Jin Li1,3,4

1 Laboratory for Reproductive Immunology, Hospital and Institute of Obstetrics and Gynecology, Fudan University Shanghai Medical College, Shanghai 200011, PR China 2 Department of Obstetrics and Gynecology, Zhongnan Hospital of Wuhan University, Wuhan 430071, PR China 3 Department of Obstetrics and Gynecology, Hainan Medical College Affiliated Hospital, Haikou 570102, PR China

4 Correspondence address. Tel/Fax: +86-21-63457331; E-mail: dmrlq1973{at}yahoo.com.cn (M-R.D.)/djli{at}shmu.edu.cn (D-J.L.)

BACKGROUND: The precise mechanisms in the materno-fetal dialogue still remain unclear. The aim of this study was to investigate the role of the chemokine CXCL12 and its receptor CXCR4 in the interaction of trophoblasts and decidual stromal cells (DSCs).

METHODS: Expression of CXCL12/CXCR4 in trophoblasts and DSCs was detected by reverse transcription–polymerase chain reaction and immunochemical staining. The secretion of CXCL12 by trophoblasts was determined by enzyme-linked immunosorbent assay. The effects of CXCL12 on the biological functions of trophoblasts and DSCs were analyzed using a cell viability assay, matrigel invasion assay and zymography. Finally, a co-culture model was established to investigate the modulation of CXCL12/CXCR4 in the interaction of trophoblasts and DSCs.

RESULTS: CXCR4 was transcribed and translated by both human trophoblasts and DSCs. Human trophoblasts secreted CXCL12 spontaneously in vitro, but DSCs did not. CXCL12 induced an apparent increase in the invasiveness of trophoblasts (P < 0.01), and up-regulated matrix metalloproteinase (MMP) 9 and MMP2 activity of both trophoblasts and DSCs (both P < 0.01) in an autocrine and paracrine manner. The invasiveness and MMP9 and MMP2 activity of trophoblasts in co-culture with DSCs increased significantly (P < 0.01), and these could be inhibited by anti-CXCR4 neutralizing antibody.

CONCLUSIONS: CXCL12 secreted by human trophoblasts enhances the coordination between trophoblasts and DSCs, via the regulation of MMP9 and MMP2, which may improve the functional materno-fetal interface.

Key words: chemokine/chemokine receptor/trophoblast cell/decidual stromal cell/materno-fetal interface

Submitted on December 9, 2007; resubmitted on July 9, 2008; accepted on July 16, 2008.


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?




Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.