Inhibition of early luteal angiogenesis by gonadotropin-releasing hormone antagonist treatment in the primate

Citation
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
Citations number
33
Categorie Soggetti
Endocrynology, Metabolism & Nutrition","Endocrinology, Nutrition & Metabolism
Journal title
JOURNAL OF CLINICAL ENDOCRINOLOGY AND METABOLISM
ISSN journal
0021972X → ACNP
Volume
85
Issue
6
Year of publication
2000
Pages
2339 - 2344
Database
ISI
SICI code
0021-972X(200006)85:6<2339:IOELAB>2.0.ZU;2-5
Abstract
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.