Fa threshold in medinria for mice brain6/12/2023 Fertil Steril 2011 95:663–666.Īmargant F, Manuel SL, Tu Q, Parkes WS, Rivas F, Zhou LT, Rowley JE, Villanueva CE, Hornick JE, Shekhawat GS. Age-related normogram for antral follicle count: McGill reference guide. AMH, anti-Müllerian hormone DAB, diaminobenzidine.Īlmog B, Shehata F, Shalom-Paz E, Tan SL, Tulandi T. The ratios of non-atretic primary and secondary follicles and similar-sized stromal cavities containing cleaved-caspase-3 positive degenerating oocytes or granulosa cells were assessed by Fisher’s exact test ( G), follicle counts were obtained from n = 4 mice per group. Cleaved caspase-3 was commonly found in a small number of granulosa cells (black arrows) in healthy developing follicles, serving as an internal positive control ( F). Numerous primary follicle-sized empty cavities were also observed (D, asterisk) and were shown to contain the remnants of zonae pellucidae via haematoxylin and eosin staining ( E, asterisks). The cleaved caspase-3 immunostaining was observed in the granulosa cells of primordial follicles ( B) and in the granulosa cells ( C, black arrow) or oocytes ( D, black arrow) of primary/secondary follicles at more-advanced stages of atresia. Cleaved (activated) caspase-3 immunoreactivity (brown DAB staining with blue haematoxylin counter stain) was not readily apparent in primordial (black arrowhead) and transitioning (white arrowhead) follicles ( A). Published by Oxford University Press on behalf of European Society of Human Reproduction and Embryology.įollicle atresia in AMH-overexpressing ( Thy1.2-AMH Tg/0) mice. ![]() No competing interests to declare.ĪMH anti-Müllerian hormone atresia follicle development folliculogenesis ovarian follicle ovary preantral follicle. This study was funded by the Health Research Council of New Zealand and the University of Otago. While this study may demonstrate a new function for AMH, the biological purpose of this function requires further investigation, particularly in mono-ovulatory species. This suggests that the role of AMH is not to conserve the ovarian reserve to prolong fertility, but instead to prevent the antral follicle pool from becoming too large. This study is consistent with prior studies showing that Amh-/- mice have increased primordial follicle activation but these new findings demonstrate that AMH-mediated preantral follicle atresia is a predominant cause of the increased small antral follicle counts in Amh-/- mice. The findings were shown only in one species and additional research will be required to determine generalizability to other species. Cleaved caspase-3 immunohistochemistry in Thy1.2-AMHTg/0 ovaries revealed high rates of granulosa cell and oocyte apoptosis in late primary/early secondary follicles of Thy1.2-AMHTg/0 mice. Despite this, Amh+/+ mice had fewer primary, secondary, small antral and medium antral follicles than Amh-/- mice indicating differing rates of developing follicle atresia between genotypes. These counteracting effects led to equivalent numbers of primordial follicles transitioning to the primary stage in Amh+/+ and Amh-/- mice. Evidence for increased rates of preantral follicle atresia was assessed by active caspase-3 immunohistochemistry in wild-type and Thy1.2-AMHTg/0 mice.Īmh -/- mice at 100-120 days of age had lower primordial follicle counts but higher primordial follicle activation rates compared to Amh+/+ mice. After confirming that follicle development speeds were identical (proliferating cell nuclear antigen immunohistochemistry), the ratio of follicles surviving beyond each stage of folliculogenesis was determined in both genotypes. The follicle counts were conducted for primordial, transitioning, primary, secondary and antral follicles in Amh-/- and Amh+/+ mice. ![]() Studies were conducted on female wild-type (Amh+/+), AMH-knockout (Amh-/-) and AMH overexpressing (Thy1.2-AMHTg/0) mice on a C57Bl/6J background (age: 42-120 days). Participants/materials, setting, methods: Our previous study showed that AMH-overexpressing mice had fewer preantral follicles than expected after accounting for primordial follicle inhibition but the reason for this was not determined.Ĭross-sectional-control versus transgenic/knockout mouse studies were carried out. Most prior studies have investigated the ability of AMH to inhibit primordial follicle activation. The present findings suggest that AMH-mediated follicle atresia only occurs in early follicles before they become sensitive to FSH. Does anti-Müllerian hormone (AMH) induce preantral follicle atresia in mice?
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