Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01178 (oxytocin)
15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied the action of GH on the production of hormones, growth factors, growth factor-binding protein and the occurrence of apoptosis in bovine ovarian granulosa cells, as well as the role of cAMP-stimulated protein kinase A (PKA) in the mediation of these effects. For this purpose we investigated the effects of exogenous bovine GH (0.001-10 microgram/ml), PKA blockers KT5720 (100 ng/ml) and adenosine-3',5'-monophosphothiodate (Rp-cAMPS) (1 micromol), alone and in combination, on IGF-I, IGF-binding protein (IGFBP)-3, oxytocin, progesterone and estradiol secretion, cAMP and PKA content and the occurrence of apoptosis. The secretion of hormones, IGF-I and IGFBP-3 into the culture medium was measured using RIA/IRMA. The presence of PKA was detected using immunocytochemistry and Western immunoblotting. The presence of cAMP in cells was demonstrated using immunocytochemistry, whilst the proportion of apoptotic cells was determined by the TUNEL method. It was found that the addition of GH to the culture medium strongly (P<0.05) stimulated IGF-I (at a concentration of 0.001-10 microgram GH/ml medium), IGFBP-3 (0.001-1 microgram GH/ml) and oxytocin (0.01-10 microgram GH/ml) secretion. Low concentrations (1-100 ng/ml) of GH stimulated, whilst a higher concentration (10 microgram/ml) inhibited estradiol output. GH slightly (P<0.05) inhibited progesterone (1-100 ng GH/ml) secretion and significantly (P<0.05) decreased the incidence of apoptosis (0.01-1 microgram GH/ml) in cultured cells. The addition of GH (100 ng/ml) caused a dramatic (P<0.05) increase in the proportion of cells possessing the immunoreactive catalytic subunit of PKA and a slight decrease in the proportion of cells containing the regulatory PKA subunit.PKA blockers KT5720 and Rp-cAMPS significantly (P<0.05) reduced the proportion of granulosa cells containing cAMP, and the catalytic and (in the case of KT5720) regulatory subunits of PKA. KT5720 given alone significantly (P<0.05) inhibited the secretion of IGFBP-3, but not that of IGF-I or progesterone. Rp-cAMPS decreased (P<0.05) the secretion of oxytocin but not that of estradiol output or the occurrence of apoptosis. KT5720 and Rp-cAMPS fully or partially prevented the GH effect on IGF-I, IGFBP-3, oxytocin, progesterone, estradiol and apoptosis. These observations suggest the involvement of GH and a cAMP/PKA-dependent intracellular cascade in the control of IGF-I, IGFBP-3, oxytocin, progesterone, estradiol, cAMP and apoptosis in bovine ovarian granulosa cells. The stimulation of PKA by GH and the prevention of GH-induced effects by PKA blockers suggest that the observed GH effects on bovine ovarian cells are probably mediated by the cAMP/PKA system.
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PMID:GH regulates secretory activity and apoptosis in cultured bovine granulosa cells through the activation of the cAMP/protein kinase A system. 1055 82

The aim of our studies was to examine whether IGF-binding protein (IGFBP)-4 is involved in the control of the secretion of various ovarian substances and also the mediation of the effects of several hormones and growth factors on this secretion. For this purpose, we carried out the transfection of porcine granulosa cells with a cDNA sense construct, increasing IGFBP-4 synthesis. We then compared the release of IGFBP-3, progesterone, oxytocin and IGF-I by control and transfected cells cultured with and without porcine LH (100 ng/ml), porcine GH (100 ng/ml), IGF-I (10 ng/ml), oxytocin (10 ng/ml) and estradiol-17beta (100 ng/ml). The concentration of IGFBP-4 produced was assessed using ligand blotting, and the release of progesterone, oxytocin, IGF-I and IGFBP-3 was evaluated using RIA/IRMA techniques. It was observed that GH, IGF-I, estradiol, LH and oxytocin alter the progesterone, oxytocin, IGF-I and IGFBP-3 release by porcine ovarian granulosa cells. Transfection of these cells with an IBFBP-4 cDNA expression construct significantly increased the IGFBP-4 accumulation in cell-conditioned medium. Furthermore, this transfection significantly reduced progesterone, oxytocin and IGFBP-3 release, and increased IGF-I output in cells cultured in the absence or presence of GH, IGF-I, estradiol and LH. The addition of oxytocin, but not of other tested substances, fully or partially prevented the effects of IGFBP-4 overexpression on IGFBP-3, IGF-I, but not on progesterone release. The present results suggested that IGFBP-4, as well as GH, IGF-I, estradiol, LH and oxytocin, is a potent regulator of porcine ovarian steroid (progesterone), nonapeptide hormone (oxytocin), growth factor (IGF-I) and growth factor-binding protein (IGFBP-3) release. IGFBP-4 is an inhibitor of basal progesterone, oxytocin and IGFBP-3 release and a stimulator of IGF-I output by porcine ovarian cells. The action of IGFBP-4 on the ovary can be mediated by (1) inhibition of oxytocin release, (2) suppression of receptor/postreceptor events induced by other hormones and IGF-I and (3) stimulation of IGF-I release.
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PMID:The transfection-induced overexpression of IGF-binding protein-4 affects the secretory activity of porcine ovarian granulosa cells and their response to hormones and IGF-I. 1135 60

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.
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PMID:Do GH, IGF-I and oxytocin interact by regulating the secretory activity of porcine ovarian cells? 1173 13