Investigation of mono-ovulatory mechanisms through the action of the inhibin/activin family

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The importance of local factors to modulate folliculogenesis has been recognized, although the key role of gonadotropins in folliculogenesis remains. We investigated the mechanisms through which local factors including activin modulated folliculogenesis.Granulosa cells from DES primed immature rats were used. The secretion of activin-A from granulosa cells increased during the culture but FSH suppressed this increase. It is suggested that this suppression occurs through cAMP/kinase A pathway because 8-Br-cAMP suppressed activin-A secretion in the same manner as FSH. IGF-I increased FSH-induced LH receptor mRNA. It is suggested that IGF-I changed the stability of LH receptor mRNA because the rate of LH receptor mRNA gene transcription was not changed but the half-life of LH receptor mRNA increased by IGF-I. PRL suppressed LH receptor expression induced by FSH after 5 days of culture. PRL did not affect LH receptor gene transcription. It was suggested that the effect of PRL was exerted by changing the stability of LH receptor mRNA. We detected adrenomedullin mRNA in granulosa cells. FSH suppressed the expression of adrenomedullin and hCG enhanced the effect of FSH. 8-Br-c AMP suppressed the expression of adrenomedullin but PMA did not have any effect on the expression. These data indicate that the differentiation of granulosa cells mediated by gonadotropins were associated with the suppression of adrenomedullin expression through a cAMP-dependent mechanism. Adrenomedullin may play a role in the process of granulosa cell differentiation as a local regulator through an autocrine/paracrine mechanism.The oocyte-granulosa-theca cell complex from immature mice secreted androstenedione by hCG and IR- inhibin and estradiol by activin-A. On the other hand, the secretion of androstenedione and estradiol was below detectable limits in the oocyte-granulosa cell complex.These results indicate that many growth factors including activin modulate folliculogenesis.