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BOR - Papers in Press, published online ahead of print October 4, 2002.
Biol Reprod 2002, 10.1095/biolreprod.102.006700
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Biology of Reproduction 67, 1804-1810 (2002)
DOI: 10.1095/biolreprod.102.006700 © 2002 Society for the Study of Reproduction, Inc.

Female Reproductive Tract

Inhibition of Vascular Endothelial Growth Factor/Vascular Permeability Factor Action Blocks Estrogen-Induced Uterine Edema and Implantation in Rodents1

L. Christie Rockwell2,a, Suresh Pillaia, C. Erik Olsona, and Robert D. Koosa

a Department of Physiology, University of Maryland School of Medicine, Baltimore, Maryland 21201

Estrogen induces a rapid increase in microvascular permeability in the rodent uterus, leading to stromal edema and a marked increase in uterine wet weight. This edema is believed to create an environment optimal for the growth and remodeling of the endometrium in preparation for implantation and pregnancy. Increased endometrial microvascular permeability also occurs in conjunction with implantation. Estrogen-induced uterine edema is immediately preceded by an increase in the expression of vascular endothelial growth factor (VEGF), a potent stimulator of microvascular permeability. The objective of this study was to determine to what degree immunoneutralization of VEGF would interfere with a) estradiol-induced uterine edema and b) pregnancy. In the first set of experiments, immature female rats were injected with either VEGF antiserum or normal rabbit serum (NRS) prior to 17ß-estradiol treatment. Rats treated with estradiol alone showed a 57% increase in uterine wet weight at 6 h compared with controls. Injection of 200 or 300 µl of VEGF antiserum reduced the response to only 20% and 10% above controls, respectively. In the second set of experiments, young adult female mice were treated with 100 µl of either VEGF antiserum or NRS at 1200 h on the fourth day after mating. NRS-treated mice had normal pregnancies. VEGF antiserum, however, completely blocked pregnancy. When VEGF antiserum-treated females were examined on Day 5 for the presence of implantation sites, none were found. These results show that a) VEGF is the major mediator of estrogen-induced increase in uterine vascular permeability and b) VEGF-induced edema is absolutely essential for implantation to take place.

1 This research was supported by NIH/NCI grant CA45055, with a supplement from the Office of Research on Women's Health, Agreement U54 HD36207 (Specialized Cooperative Center in Reproduction Research at the University of Maryland School of Medicine as part of the NICHD's Specialized Cooperative Centers Program in Reproduction Research), and NIH/NICHD Institutional Training Grant HD07170. Preliminary reports of this work were presented at the 31st annual meeting of the Society for the Study of Reproduction, Portland, OR, 1998, and at the 34th annual meeting of the Society for the Study of Reproduction, Ottawa, Canada, 2001.

2 Correspondence and current address: L. Christie Rockwell, Department of Anthropology, Temple University, 1115 W. Berks Street, Philadelphia, PA 19122. FAX: 215 204 1410; lrockwel{at}temple.edu




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