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Mol. Hum. Reprod. Advance Access published online on March 4, 2005
Molecular Human Reproduction, doi:10.1093/molehr/gah160
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Molecular Human Reproduction © European Society of Human Reproduction and Embryology 2005; all rights reserved
Received December 15, 2004
Accepted January 30, 2005

Article

HCG increases trophoblast migration in vitro via the insulin-like growth factor-II/mannose-6 phosphate receptor

M. Zygmunt 1*, T. McKinnon 2, F. Herr 3, P.K. Lala 4, and V.K. M. Han 5

1 MRC Group in Fetal and Neonatal Health and Development, The Lawson Research Institute and The Child Health Research Institute, University of Western Ontario, London, Ontario, Canada; Department of Obstetrics and Gynecology, University of Giessen, Germany
2 Department of Anatomy and Cell Biology, University of Western Ontario, London, Ontario, Canada; Department of Obstetrics and Gynecology, University of Giessen, Germany
3 Department of Obstetrics and Gynecology, University of Giessen, Germany
4 Department of Anatomy and Cell Biology, University of Western Ontario, London, Ontario, Canada
5 MRC Group in Fetal and Neonatal Health and Development, The Lawson Research Institute and The Child Health Research Institute, University of Western Ontario, London, Ontario, Canada; Department of Pediatrics and Biochemistry, University of Western Ontario, London, Ontario, Canada; Department of Anatomy and Cell Biology, University of Western Ontario, London, Ontario, Canada

* To whom correspondence should be addressed.
M. Zygmunt, E-mail: marek.t.zygmunt{at}gyn.med.uni-giessen.de


  Abstract

We have previously shown that both HCG and insulin-like growth factor-II (IGF-II) stimulate trophoblastic invasion. Furthermore, the invasion-promoting function of IGF-II resulted from IGF-II mannose 6-phosphate receptor (IGF-II/M6PR) activation. Since HCG and IGF-II did not have an additive effect on cell migration of extravillous trophoblast (EVT) cell line, HTR-8 SVneo, we hypothesized that HCG actions are mediated via alterations in the expression and/or function of IGF-II axis. HCG treatment (50-50 000 mU/ml) of the HTR-8/SVneo cells did not alter the expression of either insulin-like growth factor-I or IGF-II mRNA or peptide synthesis, but caused (i) an increase in the 125I-IGF-II binding to EVT cells, and (ii) an increase in the externalization rate of the IGF-II binding sites without affecting their internalization. This effect was due to the increase in the number of IGF-II binding sites in the plasma membrane without any change in the IGF-II binding affinity. Although HCG did not influence the abundance of IGF-II/M6PR mRNA or protein, anti-IGF-II/M6PR antibody decreased HCG-induced migration of EVT, supporting the hypothesis that HCG might stimulate EVT migration by increasing IGF-II binding to the plasma membrane and subsequently by increasing the IGF-II effect probably mediated via the IGF-II/M6PR.

Keywords: HCG; insulin-like growth factor-II; IGF-II receptor; trophoblast migration; receptor recycling.

This work was supported by grants from the German Research Council (DFG; to M.Z. Zy 19/2-1, Zy 19/3-1) and the Medical Research Council of Canada (MRC; to V.K.M.H. and P.K.L.).


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