4.5 Article

Expression of anti-Mullerian hormone protein during early follicular development in the primate ovary in vivo is influenced by suppression of gonadotropin secretion and inhibition of vascular endothelial growth factor

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ENDOCRINOLOGY
卷 148, 期 5, 页码 2273-2281

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ENDOCRINE SOC
DOI: 10.1210/en.2006-1501

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  1. Medical Research Council [MC_U127684437] Funding Source: Medline
  2. MRC [MC_U127684437] Funding Source: UKRI
  3. Medical Research Council [MC_U127684437] Funding Source: researchfish

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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 vascular endothelial growth factor ( VEGF) activity on AMH expression in vivo. GnRH antagonist or VEGF Trap, a soluble decoy receptor, was administered on d 0 or 5 of the follicular phase of the cycle, and ovaries were collected at the end of the follicular phase ( d 10). AMH protein was expressed in the marmoset ovary in granulosa cells from the primary stage, with the most abundant staining at the pre- antral and early antral stages. Inhibition of gonadotropin secretion or VEGF activity between d 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 d 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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