Human Reproduction, Vol 12, 1280-1292, Copyright © 1997 by Oxford University Press
RR Greb, O Heikinheimo, RF Williams, GD Hodgen and AL Goodman
We investigated hormonal regulation of endometrial angiogenesis in
menstruating primates. This study was designed to demonstrate: (i) that
cell-specific vascular endothelial growth factor (VEGF) production and
expression in monkey endometrium are regulated by steroid receptor ligands;
and (ii) mifepristone (RU 486) alters VEGF production even in the absence
of a progestin agonist. Endometrial VEGF production was compared by
computer-assisted immunohistochemical analysis during induced
hypoestrogenism and after oestradiol, progestin, or antiprogestin
(mifepristone) treatment. VEGF gene expression was estimated by
quantitative reverse-transcriptase polymerase chain reaction (RT-PCR) in
endometrial samples from castrate cynomolgus monkeys, from intact monkeys
in the luteal phase, and from monkeys treated for 20 days with
levonorgestrel (LNG) or mifepristone. VEGF staining intensities in
glandular epithelium and VEGF mRNA expression were highest in
hypoestrogenic monkeys. Progestin treatment induced intense VEGF staining
in the stroma. Gene expression of VEGF-189, but not other isoforms, was
higher in progesterone- and progestin (LNG)- exposed endometria compared to
mifepristone-exposed endometria or endometria from anovulatory cycles (P
< 0.04). Mifepristone abolished VEGF staining in glandular epithelium
almost completely. We conclude that VEGF protein and VEGF mRNA expression
levels in primate endometrium depend on the steroidal milieu.
Anti-angiogenic effects of mifepristone via suppression of VEGF production
might represent a mechanism for its quelling effects on endometrium.
ARTICLES
Vascular endothelial growth factor in primate endometrium is regulated by oestrogen-receptor and progesterone-receptor ligands in vivo
The Jones Institute for Reproductive Medicine, Department of Obstetrics and Gynecology, Eastern Virginia Medical School, Norfolk 23507, USA.
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