PROLACTIN DELAYS GONADOTROPIN-INDUCED OVULATION AND DOWN-REGULATES EXPRESSION OF PLASMINOGEN-ACTIVATOR SYSTEM IN OVARY

This study was conducted to determine whether prolactin (PRL) suppress es gonadotrophin-induced ovulation and disturbs the co-ordinated gene expression of tissue type plasminogen activator (tPA) and plasminogen activator inhibitor type-1 (PAI-1) in rat ovary, Immature female rats were injected with 10 IU pregnant mare's serum gonadotrophin to stimul ate follicle growth, and 48 h received different doses of prolactin fo llowed by 7 IU human chorionic gonadotrophin (HCG). The oviducts were examined for the presence of ova, and the amounts of tPA and PAI-1 mRN A present in the ovary were measured at various times after the hormon e treatment, PRL had no significant effect on ovarian weight but cause d a dose-dependent decrease in ovulation number, In the control animal s receiving HCG alone, 13.3 +/- 1.3 (mean +/- SEM) ova/oviduct were fo und; while in animals receiving HCG plus 50, 100 or 200 mu g PRL, the ovulation number was dose-dependently suppressed by 53.6, 66.9 and 76% respectively at 18 h after treatment, PRL suppression of HCG-induced ovulation was time-dependent. By 24 h after treatment, the number of o va in the oviducts in HCG-and HCG plus PRL-treated groups was not sign ificantly different, PRL also suppressed HCG-induced tPA gene expressi on in a dose-and time-dependent manner, At all time points examined, t PA mRNA content of whole ovaries and granulosa cells (GC) in PRL-treat ed groups was lower than in the HCG-treated controls, The activities o f PAI-1 in ovarian extracellular fluid (OEF) and PAI-1 mRNA in the the ca-interstitial cells (TI) in the PRL-treated groups were higher than in the HCG-treated controls, The highest stimulation by PRL of PAI-1 a ctivity in OEF and of PAI-1 mRNA in TI was observed at 9 h and 6 h aft er HCG treatment respectively, The localization of tPA and PAI-1 antig ens in the ovaries was consistent with changes in the mRNA and activit y levels, These data suggest that PRL temporarily delays, but does not completely inhibit, HCG-induced ovulation, which may be caused by a s uppression of PA-mediated proteolysis.