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Endocrine Gland-Derived Vascular Endothelial Growth Factor Is Expressed in Human Peri-implantation Endometrium, But Not in Endometrial Carcinoma

Departments of Surgery (E.S.W.N., K.Y.L.) and Obstetrics and Gynecology (W.S.B.Y., H.Y.S.N., E.H.Y.N., P.C.H.), University of Hong Kong, Pokfulam, Hong Kong

Address all correspondence and requests for reprints to: Dr. Elly S. W. Ngan, Research Assistant Professor, Department of Surgery, University of Hong Kong, Pokfulam, Faculty of Medicine Building, 21 Sassoon Road, Hong Kong, SAR, China. E-mail: engan{at}hkucc.hku.hk.

Endocrine gland-derived vascular endothelial growth factor (EG-VEGF) is a newly identified angiogenic and permeability-enhancing factor, predominantly expressed in steroidogenic tissues. Recently, we found that EG-VEGF is also expressed in the normal peri-implantation endometrial samples from patients of reproductive ages (80%). Immunohistochemistry analysis showed that EG-VEGF is predominantly expressed in the glandular epithelial cells and its expression is dynamic during the menstrual cycle with a peak expression at the mid-luteal phase. We also found that EG-VEGF transcripts are up-regulated in all the peri-implantation endometrial samples from the patients after the ovulating dose of human chorionic gonadotropin in gonadotropin-stimulated cycles and patients receiving hormone replacement therapy. In in vitro endometrial cell culture, EG-VEGF mRNA was detected in endometrial cells only in the presence of steroids, suggesting that EG-VEGF expression is highly dependent on the steroid hormones. Subsequent expression analyses on the EG-VEGF receptors showed that hPK-R1 and hPK-R2 are differentially expressed in human endometrium, but show no significant correlation with the hormonal treatments. On the other hand, EG-VEGF transcript was rarely detected in the endometrial samples from the postmenopausal patients and patients with endometrial carcinoma. It may imply that EG-VEGF may only play a role in vascular function of peri-implantation endometrium, but is unlikely to be associated with the etiology of endometrial cancer development.

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