Do GH, IGF-I and oxytocin interact by regulating the secretory activity of porcine ovarian cells?
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.
Sirotkin
A V
AV
Research Institute of Animal Production, 949 92 Nitra, Slovakia. sirotkin@vuzv.sk
Makarevich
A V
AV
Kwon
H B
HB
Kotwica
J
J
Bulla
J
J
Hetényi
L
L
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*
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