Regulation of VEGF in the reproductive tract by sex-steroid hormones

S.M. Hyder and G.M. Stancel

Department of Integrative Biology and Pharmacology, The University of Texas Medical School at Houston, Houston, USA

Offprint requests to: Dr. Salman M. Hyder, Department of Integrative Biology and Pharmacology, University of Texas Health Sciences Center, 6431 Fannin Street, Houston, TX 77030, USA. Fax: 713-500-7455. e-mail: shyder@farmr1.med.uth.tmc.edu

Summary. Vascular endothelial growth factor (VEGF) is a key regulator of angiogenesis. In adults, angiogenesis is an infrequent event in the normal tissue except in the female reproductive tract where angiogenesis occurs frequently during the cyclical repair and regeneration of the endometrium as well as in the ovary. Little is known about angiogenesis in the male reproductive tract. The role of VEGF in controlling reproductive tract physiology and the role of hormones in regulating this key regulator of angiogenesis is not well understood. Since reproductive tract physiology is largely under sex-steroid regulation, we have reviewed some recent studies describing the role of sex-steroid hormones in regulating VEGF. We have also included studies on the role of sex-steroids in regulating VEGF and angiogenesis in endometrial, breast and prostate pathologies. We have provided an extensive review of the classical VEGF and VEGF receptors with examples drawn from numerous studies in the literature using diverse biological systems to encourage similar studies in the area of reproductive tract physiology. It is speculated that such studies will provide insights into understanding the role of VEGF in reproductive tract development, causes of infertility, and cancer. Such knowledge would allow us to target VEGF for improving human reproductive tract abnormalities, for enhancing implantation and fertility, and for designing drugs for treatment of endocrine dependent cancers. Histol. Histopathol. 15, 325-334 (2000)

Key words: Vascular endothelial growth factor, Angiogenesis, Cancer, Estrogen, Progestin, Androgen, Steroid receptors

DOI: 10.14670/HH-15.325