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BOR - Papers in Press, published online ahead of print August 11, 2004.
Biol Reprod 2004, 10.1095/biolreprod.104.032722
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BIOLOGY OF REPRODUCTION 71, 1963–1967 (2004)
DOI: 10.1095/biolreprod.104.032722
© 2004 by the Society for the Study of Reproduction, Inc.

Pregnancy

The Effect of Leptin on Mouse Trophoblast Cell Invasion1

Laura C. Schulz2, and Eric P. Widmaier

Department of Biology, Boston University, Boston, Massachusetts 02215

The hormone leptin is produced by adipose tissue and can function as a signal of nutritional status to the reproductive system. The expression of leptin receptor and, in some species, leptin, in the placenta suggests a role for leptin in placental development, but this role has not been elucidated. Leptin is required at the time of embryo implantation in the leptin-deficient ob/ ob mouse and has been shown to upregulate expression of matrix metalloproteinases (MMPs), enzymes involved in trophoblast invasion, in cultured human trophoblast cells. This led us to the hypothesis that leptin promotes the invasiveness of trophoblast cells crucial to placental development. We found that leptin stimulated mouse trophoblast cell invasion through a matrigel-coated insert on Day 10, but not Day 18 of pregnancy. Optimal stimulation occurred at a concentration of 50 ng/ml leptin, similar to the peak plasma leptin concentration during pregnancy in the mouse. Leptin treatment did not stimulate proliferation of mouse trophoblast cells in primary culture. Leptin stimulation of invasion was prevented by 25 µM GM6001, an inhibitor of MMP activity. Our results suggest that leptin may play a role in the establishment of the placenta during early pregnancy and that this function is dependent on MMP activity. This effect of leptin may represent one mechanism by which body condition affects placental development.

1 Supported by NSF IBN0131846 and National Research Service Award, NIH 1 F32 HD45116–01A1.

2 Correspondence: Laura C. Schulz, 5 Cummington St., Boston, MA 02215. FAX: 617 353 6041; lcschulz{at}bu.edu






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Copyright © 2004 by the Society for the Study of Reproduction.