| Co-Investigator(Kenkyū-buntansha) |
IGARASHI Toshio Teikyo University, Department of Medicine, Lecturer, 医学部附属市原病院, 講師 (10311622)
SUENAGA Akihiko Saitama Medical College, Department of Medicine, Assistant, 総合医療センター, 助手 (10302712)
OKAGAKI Ryugo Saitama Medical College, Department of Medicine, Lecturer, 医学部, 講師 (00302711)
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| Research Abstract |
1.The expression levels of inhibin, activin, and follistatin mRNA were measured in granulose cells (GCs) obtained from IVF-ET patients, which were consequently evaluated if there was any relationship with several clinical parameters. As a result inhibin a-subunit mR.NA level was higher in follicles which contained maturing oocytes. However it was lower in follicles from which high quality embryos were obtained. This suggests though expression of inhibin a=subunit is necessary for oocyte maturation, its too much expression causes negative effect on embryos.
2.Follicles of either normal cycling women or polycystic ovarian syndrome (PCOS) patients were transvaginally aspirated and both follicular fluid (FF) and GCs were obtained. Protein levels of inhibin (A or B), activin A, free follistatin and several steroid hormones (androstenedione, estradiol, rogesterone) in FF as well as niR.NA levels of inhibin subunits (a, (3A, (3B), follistatin subtypes (288 and 315) were measured. In normal cycling women androstenedione was high, while estradiol was low in FF of small follicles. As follicles grew, the fonner decreased, while the latter increased. Both itt ibin A and progesterone showed increase following. follicular growth, whereas inhibin B, activin A, free follistatin levels did not change significantly. In the levels of rnRNA, both inhibin a and (3A-subunit showed increase along with follicular growth, whereas neither inhibin (3B-subunit nor follistatin 288/315 changed significantly. In PCOS GCs ni NA levels of both inhibin subunit-a and (3A were significantly lower compared to those of size matched follicles. The other mRNA did not show significant difference. These findings imply the possible involvement of inhibin/activtn system in pathophysiology of PCOS.
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