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Medical Research Council Reproductive Biology Unit, Center for Reproductive Biology (H.M.F., S.E.D., S.F.L., C.W., K.D.M.), Edinburgh, United Kingdom EH3 9ET; the Department of Cancer Medicine, Imperial College School of Medicine, Hammersmith Campus (V.A.C.), London, United Kingdom W12 0NN; and Molecular Angiogenesis Laboratories, Imperial Cancer Research Fund, Institute of Molecular Medicine, John Radcliffe Hospital (R.B.), Oxford, United Kingdom OX3 9DS
Address all correspondence and requests for reprints to: Dr. H. M. Fraser, Medical Research Council, Reproductive Biology Unit, Center for Reproductive Biology, 37 Chalmers Street, Edinburgh, United Kingdom EH3 9EW. E-mail: h.fraser{at}ed-rbu.mrc.ac.uk
Manipulation of angiogenesis may have a profound effect on female reproductive function, but this has not yet been demonstrated by direct experiment in species with ovulatory cycles similar to those in women. To investigate whether angiogenesis could be inhibited in the primate corpus luteum, and the consequences of such inhibition on luteal function, marmosets were treated with an antibody to vascular endothelial growth factor (VEGF). Treatment commenced at the time of ovulation and was continued for 3 days (early luteal group) or 10 days (midluteal group). Bromodeoxyuridine was used to label proliferating cells, being administered 1 h before collecting ovaries from control and treated animals in the early or midluteal phase. Ovarian sections were stained using an antibody to bromodeoxyuridine, and a proliferation index was obtained; endothelial cell quantification was performed using factor VIII as an endothelial cell marker. Intense proliferation in the early luteal phase was suppressed by anti-VEGF treatment. This resulted in blockade of development of the normally extensive capillary bed, as in the animals treated until the mid-luteal phase the numbers of endothelial cells were reduced. The hormone-producing cells remained largely unaltered in the posttreatment corpus luteum, although the presence of lipid accumulation, and small pockets of cells showing basophilia and nuclear condensation were observed. Significantly, luteal function, as judged by secretion of progesterone, was markedly compromised by the treatment, being reduced by 60% in comparison with controls. It is concluded that VEGF-mediated angiogenesis is an essential component of luteal function in primates and therefore has the potential to be regulated.
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L. P. Reynolds and D. A. Redmer Angiogenesis in the Placenta Biol Reprod, April 1, 2001; 64(4): 1033 - 1040. [Abstract] [Full Text]
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C. Wulff, H. Wilson, P. Largue, W. C. Duncan, D. G. Armstrong, and H. M. Fraser Angiogenesis in the Human Corpus Luteum: Localization and Changes in Angiopoietins, Tie-2, and Vascular Endothelial Growth Factor Messenger Ribonucleic Acid J. Clin. Endocrinol. Metab., November 1, 2000; 85(11): 4302 - 4309. [Abstract] [Full Text]
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 S. Hague, L. Zhang, M. K. Oehler, S. Manek, I. Z. MacKenzie, R. Bicknell, and M. C. P. Rees Expression of the Hypoxically Regulated Angiogenic Factor Adrenomedullin Correlates with Uterine Leiomyoma Vascular Density Clin. Cancer Res., July 1, 2000; 6(7): 2808 - 2814. [Abstract] [Full Text]
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S. E. Dickson and H. M. Fraser Inhibition of Early Luteal Angiogenesis by Gonadotropin-Releasing Hormone Antagonist Treatment in the Primate J. Clin. Endocrinol. Metab., June 1, 2000; 85(6): 2339 - 2344. [Abstract] [Full Text]
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