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Submitted on July 28, 2004
Accepted on December 1, 2004
Department of Obstetrics and Gynecology, Division of Reproductive Endocrinology (GSN, RCZ, MVS, JK), Department of Pathology (JK), Columbia University, New York, New York, USA; ImClone Systems Incorporated (PB, FL), New York, New York, USA
* To whom correspondence should be addressed. E-mail: rcz3{at}columbia.edu.
While it has been previously demonstrated that administration of anti-VEGFR-2 antibodies to hypophysectomized(Hx) mice during gonadotropin-stimulated folliculogenesis and luteogenesis inhibits angiogenesis in the developing follicle and corpus luteum(CL), it is unclear which of the many components of VEGF inhibition are important for the inhibitory effects on ovarian angiogenesis. To examine if ovarian angiogenesis can be more specifically targeted, we administered an antibody to VE-cadherin (VE-C), an interendothelial adhesion molecule, to Hx mice during gonadotropin stimulation. In tumor models, in vivo and in vitro assays, the anti-VE-C antibody, E4G10, has been shown to specifically inhibit angiogenesis, but VE-C has yet to be inhibited in the context of ovarian angiogenesis. In addition to studying the effect on neovascularization in the follicular and luteal phases, we also examined the effect of E4G10 on established vessels of the CL of pregnancy. The results demonstrate that E4G10 specifically blocks neovascularization in the follicular and luteal phases, causing an inhibition of preovulatory follicle and CL development, a decrease in the vascular area, and an inhibition of function demonstrated by reduced hormone levels. However, when administered during pregnancy, unlike anti-VEGFR-2 antibody, E4G10 is unable to cause disruption of the established vessels of the mature CL. This data demonstrates that E4G10 causes a specific inhibition of neovascularization in the ovary without destabilizing preexisting vasculature.
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