2003 Volume 49 Issue 2 Pages 141-149
The aims of the present study were (1) to investigate the influence of insulin-like growth factor-I (IGF-I) on follicular size, on the secretion of oxytocin (OT), progesterone (P), estradiol (E), IGF binding protein-3 (IGFBP-3), inhibin A, inhibin B and cAMP and on the expression of proliferation-associated peptide PCNA, ERK-related mitogen activated protein kinase (MAPK/ERK1, 2) and protein kinase A (PKA) in cultured porcine ovarian follicles; (2) to examine the effects of OT on IGF-I and on these functions; and (3) to determine whether the effects of IGF-I can be mediated by OT. To define the involvement of OT in mediating IGF-I action, we compared responses of porcine ovarian follicles to IGF-I and OT and examined whether blockade of endogenous OT by specific antiserum can affect IGF-I action. It was observed that IGF-I (1, 10 or 100 ng/ml) was able to prevent a decrease in the size of ovarian follicles during culture and caused an increase in the diameter of some follicles. It also stimulated the secretion of OT, P, IGFBP-3, inhibin A and cAMP, decreased the secretion of E and inhibin B (RIA/EIA/ELISA), and induced the expression of PCNA, PKA, MAPK/ERK1, but not MAPK/ERK2 (Western blotting). Like IGF-1, OT (100 ng/ml) prevented decrease in follicular size and increased the diameter of some follicles. It also stimulated the secretion of P and IGF-I, but not E. Antiserum against OT (1%), when given alone, did not affect the reduction of follicular size but slightly increased the percentage of follicles increasing their diameter during culture. The antiserum also inhibited secretion of OT and cAMP but not the secretion of P, E, IGFBP-3 or the expression of PKA, MAPK/ERK1 or 2. When given together with IGF-I, the antiserum prevented the stimulatory action of IGF-I on the proportion of enlarged follicles and on OT, IGFBP-3 and MAPK/ERK1. It augmented the effect of IGF-I on P, but not the effect on E, cAMP, PKA or MAPK/ERK2. These observations demonstrate the involvement of IGF-I and OT in the control of ovarian follicular size and follicular cell proliferation, progestagen, estrogen, IGFBP-3, inhibin A and B secretion and in cAMP/PKA- and MAPK/ERK1-dependent intracellular mechanisms. Furthermore, the reciprocal stimulation of IGF-I and OT and the similarity of some their effects, together with the prevention or augmentation of some IGF-I effects after OT blockade, suggest that IGF-I action can be mediated by OT.