Se. Dickson et Hm. Fraser, Inhibition of early luteal angiogenesis by gonadotropin-releasing hormone antagonist treatment in the primate, J CLIN END, 85(6), 2000, pp. 2339-2344
Angiogenesis during luteal development is essential for normal lutein cell
function, but the control of this process and the relationships between the
steroidogenic and endothelial cells have still to be elucidated. The aim o
f this study was to: 1) quantify endothelial cell proliferation throughout
the luteal phase of the marmoset ovulatory cycle; 2) determine the effect o
f gonadotropin withdrawal using GnRH antagonist treatment on the early lute
al phase angiogenesis peak; and 3) describe the resultant morphological cha
nges in the corpus luteum (CL). Ovaries were collected during the early, mi
d-, and late luteal phase, and changes in angiogenic activity were determin
ed by quantification of bromodeoxyuridine incorporation. Animals were treat
ed with a GnRH antagonist, on luteal days 1 and 2, and ovaries were collect
ed on day 3. A proliferation index was obtained by counting the number of b
romodeoxyuridine immunopositive cells in luteal sections. Cell proliferatio
n was maximal in the early luteal phase and fell significantly in the mid-
and late CL. GnRH antagonist treatment reduced the early luteal phase proli
feration peak by 90%, suppressed plasma progesterone, and severely disrupte
d lutein cell morphology. These results demonstrate that the intense angiog
enesis in the early primate CL is dependent on gonadotropin stimulation of
lutein cells.