Skip Navigation



Hum. Reprod. Advance Access published online on February 16, 2009
Human Reproduction, doi:10.1093/humrep/dep026
This Article
Right arrow Full Text
Right arrow Full Text (PDF )
Right arrow All Versions of this Article:
24/6/1339    most recent
dep026v1
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 McCormick, J.
Right arrow Articles by Cartwright, J. E.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by McCormick, J.
Right arrow Articles by Cartwright, J. E.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

© The Author 2009. 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

Soluble HLA-G regulates motility and invasion of the trophoblast-derived cell line SGHPL-4

James McCormick1,3, Guy St J. Whitley1, Philippe Le Bouteiller2 and Judith E. Cartwright1

1 Division of Basic Medical Sciences, Developmental and Endocrine Signalling Centre, St George’s, University of London, Cranmer Terrace, London SW17 0RE, UK 2 INSERM U563, Centre de Physiopathologie de Toulouse-Purpan, Toulouse F-31300, France

3 Correspondence address. Tel: +44-208-725-5850; E-mail: j.mccormick{at}sgul.ac.uk

BACKGROUND: Soluble human leucocyte antigen-G (sHLA-G) is secreted by extravillous trophoblast (EVT) and has roles in regulating immune cells within the decidua. HLA-G expression on EVT increases as they approach uterine spiral arteries and we have suggested that sHLA-G may be important in the remodelling of these vessels. The autocrine role of sHLA-G in regulating trophoblast function at this critical phase has not been studied. We aimed to investigate the effects of sHLA-G on trophoblast motility, invasion and survival.

METHODS: The human EVT line, SGHPL-4, was stably transfected to over-express sHLA-G (SGHPL-4sG1). Motility and apoptosis were assessed by time–lapse microscopy. Cells were cultured on microcarrier beads embedded in fibrin gels to assess invasion. The effect of sHLA-G expression on motility, invasion and apoptosis in response to stimulation with either hepatocyte growth factor (HGF) or epidermal growth factor (EGF) was determined.

RESULTS: There was no difference in the motility of either SGHPL-4 cells or SGHPL-4sG1 cells in the absence of stimulation. However, sHLA-G inhibited HGF-induced EVT motility. HGF- and EGF-induced invasions were significantly inhibited in SGHPL-4sG1 compared with SGHPL-4 cells. Increased expression of HLA-G had no significant effect on tumour necrosis factor (TNF)-{alpha}/actinomycin-induced apoptosis.

CONCLUSIONS: Growth factor-stimulated trophoblast motility and invasion are regulated by sHLA-G, indicating a novel autocrine role. The inhibition of trophoblast invasion at the spiral artery may be important to allow interactions leading to vascular remodelling.

Key words: trophoblast/invasion/motility/HLA-G/placenta

Submitted on June 6, 2008; resubmitted on January 9, 2009; accepted on January 19, 2009.


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.