Inhibition of Early Luteal Angiogenesis by Gonadotropin-Releasing Hormone Antagonist Treatment in the Primate
Sarah E. Dickson and
Hamish M. Fraser
Medical Research Council Human Reproductive Sciences Unit,
Centre for Reproductive Biology, Edinburgh, EH3 9ET, United
Kingdom
Address correspondence and requests for reprints to: Sarah E. Dickson, Medical Research Council Human Reproductive Sciences Unit, Centre for Reproductive Biology, 37 Chalmers Street, Edinburgh, EH3 9ET, United Kingdom. E-mail: s.dickson{at}ed-rbu.mrc.ac.uk
Angiogenesis during luteal development is essential for normallutein
cell function, but the control of this process and therelationships
between the steroidogenic and endothelial cellshave still to be
elucidated. The aim of this study was to: 1)quantify endothelial cell
proliferation throughout the lutealphase of the marmoset ovulatory
cycle; 2) determine the effectof gonadotropin withdrawal using GnRH
antagonist treatment onthe early luteal phase angiogenesis peak; and
3) describe theresultant morphological changes in the corpus luteum
(CL). Ovarieswere collected during the early, mid-, and late luteal
phase,and changes in angiogenic activity were determined by
quantificationof bromodeoxyuridine incorporation. Animals were
treated witha GnRH antagonist, on luteal days 1 and 2, and ovaries
werecollected on day 3. A proliferation index was obtained by counting
thenumber of bromodeoxyuridine immunopositive cells in luteal
sections.Cell proliferation was maximal in the early luteal phase and
fellsignificantly in the mid- and late CL. GnRH antagonist treatment
reducedthe early luteal phase proliferation peak by 90%, suppressed
plasmaprogesterone, and severely disrupted lutein cell morphology.
Theseresults demonstrate that the intense angiogenesis in the early
primateCL is dependent on gonadotropin stimulation of lutein cells.
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