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Submitted on November 9, 2006
Accepted on February 13, 2007
Medical Research Council Human Reproductive Sciences Unit, University of Edinburgh Centre for Reproductive Biology, The Queen's Medical Research Institute, 47 Little France Crescent, Edinburgh, EH16 4TJ, UK. Institute of Cell Biology, The Darwin Building, University of Edinburgh, King's Buildings, Mayfield Road, Edinburgh EH9 3JR
* To whom correspondence should be addressed. E-mail: f.thomas{at}hrsu.mrc.ac.uk.
Anti-Mullerian hormone (AMH) plays a role during early follicular development and selection. The aim of this study was to determine the pattern of AMH protein expression in the marmoset ovary and to investigate the effects of inhibition of gonadotropins or VEGF activity on AMH expression in vivo. GnRH antagonist or VEGF Trap, a soluble decoy receptor, was administered on Day 0 or Day 5 of the follicular phase of the cycle, and ovaries were collected at the end of the follicular phase (Day 10). AMH protein was expressed in the marmoset ovary in granulosa cells from the primary stage, with the most abundant staining at the preantral and early antral stages. Inhibition of gonadotropin secretion or VEGF activity between Day 0-10 of the cycle decreased AMH expression in early preantral follicles (p<0.01), and AMH expression was decreased in late preantral follicles in the presence of the VEGF Trap (p<0.01), compared with controls. There was significantly less AMH expression in early antral follicles with both treatments (p<0.01), and a decrease in the ratio of oocyte-associated/basement membrane-associated granulosa cell expression of AMH (p<0.05). When treatments were administered from Day 5-10 of the cycle, both VEGF Trap and GnRH antagonist decreased AMH expression in preantral follicles (p<0.01), but had no significant effect on early antral follicles. In conclusion, VEGF and gonadotropins are involved in the regulation of expression of AMH in the marmoset. This AMH expression may be a marker of abnormal folliculogenesis in the absence of gonadotropin stimulation or functional angiogenesis.
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