Mol. Hum. Reprod. Advance Access originally published online on March 4, 2005
Molecular Human Reproduction 2005 11(4):261-267; doi:10.1093/molehr/gah160
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HCG increases trophoblast migration in vitro via the insulin-like growth factor-II/mannose-6 phosphate receptor
1MRC Group in Fetal and Neonatal Health and Development, The Lawson Research Institute and The Child Health Research Institute,2Department of Pediatrics and Biochemistry,3Department of Anatomy and Cell Biology, University of Western Ontario, London, Ontario, Canada and 4Department of Obstetrics and Gynecology, University of Giessen, Germany
5 To whom Correspondence should be adressed at: Department of Obstetrics and Gynecology, University of Giessen, Klinikstr 32, D-35385 Giessen, Germany. E-mail: marek.t.zygmunt{at}gyn.med.uni-giessen.de
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.
Key words: 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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