SFE2004 Oral Communications Neuroendocrinology and Reproduction (8 abstracts)
Reduced expression of anti-Mullerian hormone (AMH) protein in the androgenised sheep ovary
L Bull 1 , S Stubbs 1 , R Birch 1 , J Robinson 2 , AP Themmen 3 , JA Visser 3 , NP Groome 4 , K Hardy 1 & S Franks 1
1Institute of Reproductive and Developmental Biology, Imperial College , Hammersmith Hospital, London, UK; 2Department of Veterinary Preclinical Studies, University of Glasgow, UK; 3Erasmus Medical Centre, Rotterdam, The Netherlands; 4Oxford Brookes University, Oxford , UK.
The prenatally androgenised sheep, like the Rhesus monkey, is an informative model for polycystic ovary syndrome (PCOS). We have recently demonstrated that AMH protein is reduced in preantral follicles of PCOS ovaries (Stubbs et al, Endocrine Abstracts 2004, 7 P186 ). We hypothesized that reduced expression of AMH is an effect of androgen excess. The aim of this study was to examine AMH immunostaining in ovaries from prenatally androgen-treated and control ewes. Ovaries were taken from 20 adult (7 androgen-treated,13 controls) and 17 fetal sheep (10 androgenised, 7 controls), fixed in formalin, paraffin-blocked and sectioned for immunohistochemistry. A middle section of each ovary was stained for AMH protein using a highly specific antibody. The total number of follicles per section, their stage of development and the presence of AMH-positive staining were recorded. In all, 1189 follicles in adult and 3577 in fetal ovary sections were analysed
Androgenised ovaries showed proportionately fewer non-growing follicles and more growing follicles than control ovaries. The proportion of AMH-positive follicles increased with increasing follicle size. In both androgen-treated groups, the proportion of follicles in AMH staining was lower in non-growing and early transitional follicles (<50% cuboidal granulosa cells) than in controls. In adult ovaries, 66% primordial and early transitional follicles were AMH-positive, compared with 76% in controls (p=0.015, Fisher exact). In fetal ovaries, few follicles were AMH positive but the proportion in androgenised animals was also lower than in controls (6.5 vs 4.7%, p=0.05).
This study demonstrates, for the first time, that prenatal androgenisation is associated with changes in AMH expression in small follicles of both fetal and adult ovaries. These findings are consistent with the hypothesis that abnormal folliculogenesis in PCOS may be mediated, at least in part, by AMH and that reduced AMH expression may itself be a function of excess androgen exposure.
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Endocrine Abstracts
ISSN 1470-3947 (print) | ISSN 1479-6848 (online)
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