title: Do GH, IGF-I and oxytocin interact by regulating the secretory activity of porcine ovarian cells?
abstract: The aims of this study on porcine ovarian granulosa cells were to examine the effect of GH on oxytocin (OT), IGF-I and IGF-I receptors, IGF-binding protein-3 (IGFBP-3), progesterone and prostaglandin E (PGE), as well as to determine whether IGF-I and/or OT may be mediators of GH action. The cells were cultured either with porcine GH (pGH) (1 ng/ml to 10 microg/ml or 100 ng/ml only), antiserum against IGF-I (0.1%), antiserum against OT (0.1%) or a combination of GH (10 ng/ml) with antiserum against IGF-I or antiserum against OT (0.1%). The secretion of IGF-I, OT, IGFBP-3, progesterone and PGE was determined using RIA/IRMA, whilst the IGF-I binding sites were measured using a radioreceptor assay. It was observed that pGH increased the secretion of IGF-I and the abundance of IGF-I binding sites in granulosa cells. Furthermore, GH inhibited OT release, stimulated progesterone and PGE output, but had no significant effect on IGFBP-3 secretion. Immunoneutralization of IGF-I by antiserum against IGF-I inhibited PGE secretion, but it did not influence progesterone or IGFBP-3 secretion. Binding of OT by antiserum suppressed IGFBP-3, PGE, but not progesterone secretion. Neither immunoneutralization of IGF-I nor OT substantially prevented the effects of GH on progesterone, IGFBP and PGE. These observations demonstrate the involvement of GH, IGF-I and OT in the control of porcine ovarian secretory activity and the ability of GH to regulate IGF-I and OT production and IGF-I reception. Nevertheless, lack of correlation between the effects of GH, antiserum against IGF-I and antiserum against OT, as well as the inability of blockade of IGF-I or OT to prevent the effects of GH, suggests that IGF-I and OT, despite their dependence on GH, do not mediate GH action on ovarian cells.
authors.affiliation: Research Institute of Animal Production, 949 92 Nitra, Slovakia. sirotkin@vuzv.sk
authors.forename: A V
authors.initials: AV
authors.lastname: Sirotkin
authors.forename: A V
authors.initials: AV
authors.lastname: Makarevich
authors.forename: H B
authors.initials: HB
authors.lastname: Kwon
authors.forename: J
authors.initials: J
authors.lastname: Kotwica
authors.forename: J
authors.initials: J
authors.lastname: Bulla
authors.forename: L
authors.initials: L
authors.lastname: Hetényi
mesh_terms: D000818:Animals; D018929:Cell Culture Techniques; D017077:Culture Media, Conditioned; D005260:Female; D006107:Granulosa Cells / Q000187:drug effects* / Q000378:metabolism; D013006:Growth Hormone / Q000494:pharmacology* / Q000502:physiology; D007106:Immune Sera; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000096:biosynthesis; D007334:Insulin-Like Growth Factor I / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000502:physiology; D010121:Oxytocin / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000502:physiology; D011374:Progesterone / Q000096:biosynthesis; D011458:Prostaglandins E / Q000096:biosynthesis; D013552:Swine / Q000378:metabolism*
chemical_list: D017077:Culture Media, Conditioned; D007106:Immune Sera; D018972:Insulin-Like Growth Factor Binding Protein 3; D011458:Prostaglandins E; D011374:Progesterone; D010121:Oxytocin; D007334:Insulin-Like Growth Factor I; D013006:Growth Hormone