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New angiogenesis research from Stanford University, Medical Department outlined



December 8th, 2008

   2008 DEC 8 -- "Despite extensive literature on vascular endothelial growth factor (VEGF) expression and regulation by steroid hormones, the lack of clear understanding of the mechanisms of angiogenesis in the endometrium is a major limitation for use of antiangiogenic therapy targeting endometrial vessels. In the current work, we used the rhesus macaque as a primate model and the decidualized mouse uterus as a murine model to examine angiogenesis during endometrial breakdown and regeneration," investigators in the United States report.

   "We found that blockade of VEGF action with VEGF Trap, a potent VEGF blocker, completely inhibited neovascularization during endometrial regeneration in both models but had no marked effect on preexisting or newly formed vessels, suggesting that VEGF is essential for neoangiogenesis but not survival of mature vessels in this vascular bed. Blockade of VEGF also blocked reepithelialization in both the postmenstrual endometrium and the mouse uterus after decidual breakdown, evidence that VEGF has pleiotropic effects in the endometrium. In vitro studies with a scratch wound assay showed that the migration of luminal epithelial cells during repair involved signaling through VEGF receptor 2-neuropilin 1 (VEGFR2-NP1) receptors on endometrial stromal cells. The leading front of tissue growth during endometrial repair was strongly hypoxic, and this hypoxia was the local stimulus for VEGF expression and angiogenesis in this tissue," wrote X.J. Fan and colleagues, Stanford University, Medical Department.

   The researchers concluded: "In summary, we provide novel experimental data indicating that VEGF is essential for endometrial neoangiogenesis during postmenstrual/postpartum repair."

   Fan and colleagues published their study in Faseb Journal (VEGF blockade inhibits angiogenesis and reepithelialization of endometrium. Faseb Journal, 2008;22(10):3571-3580).

   For additional information, contact N.R. Nayak, Stanford University, School Medical, Dept. of Obstetrics & Gynecology, 300 Pasteur Dr., HH-333, Stanford, CA 94305, USA.

   The publisher of the Faseb Journal can be contacted at: Federation American Society Experimental Biology, 9650 Rockville Pike, Bethesda, MD 20814-3998, USA.

   Keywords: United States, Stanford, Angiogenesis, Hormones, Neovascularization, Oncology, Therapy, Treatment, Tumor Vascularization, VEGF, Vascular Endothelial Growth Factor, Stanford University, Medical Department.

   This article was prepared by Biotech Business Week editors from staff and other reports. Copyright 2008, Biotech Business Week via NewsRx.com.

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