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Query: UNIPROT:P01178 (oxytocin)
 15,767 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Liver regeneration following partial hepatectomy is significantly impaired in rats with hereditary vasopressin (AVP) deficiency. This suggested that AVP might have a direct effect on cultured rat hepatocytes. Hepatocytes from male Sprague-Dawley rats were isolated using a two-step collagenase perfusion technique and plated at a density of 10(5)/16-mm Primaria plate. After a suitable attachment period, hepatocytes were incubated with minimal essential media, AVP, AVP plus a specific AVP antagonist, or oxytocin. Hepatocyte proliferation was measured by [3H]thymidine incorporation ([3H]Thy) into hepatocyte DNA. AVP (10 nM) increased [3H]Thy significantly (and this effect was blocked by an AVP-specific antagonist (50 nM). Oxytocin had no effect on hepatocyte DNA synthesis. To further investigate the influence of AVP on hepatocyte proliferation, the effect of AVP on transforming growth factor-alpha (TGF-alpha)-stimulated hepatocyte proliferation was also studied. This combination was chosen based on the ability of AVP to inhibit the biologic effects of EGF (a TGF-alpha analog). There was significant attenuation of TGF-alpha (50 nM)-stimulated [3H]Thy in the presence of AVP (10 nM). In summary: (1) AVP stimulates proliferation of cultured rat hepatocytes. (2) The effect of AVP can be significantly abolished by a specific AVP antagonist. (3) The proliferative response of AVP is specific. (4) AVP significantly attenuates TGF-alpha-stimulated hepatocyte hepatic DNA synthesis. Further studies should elucidate the mechanisms for the effects of AVP on hepatic proliferation alone or in combination with other factors.
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PMID:Vasopressin stimulates DNA synthesis in cultured rat hepatocytes. 799 50

Oxytocin (OT) receptors (OTR) in rabbit amnion increase more than 200-fold at the end of gestation. In the present report, we studied the basis of this up-regulation. Incubation of amnion cells with cortisol (20 nM) for 24 h increased the amount of 125I-labeled OT antagonist bound by 16- to 18-fold. The effects of cortisol were dose and steroid dependent. Administration of glucocorticoid to pregnant does also increased the concentration of OTRs in amnion. The effects of cortisol in vitro were potentiated by the addition of forskolin (50 microM), so that OTR number increased by as much as 182 times. The effects of cortisol and forskolin, either separately or in combination, were inhibited by activation of protein kinase-C or coincubation with transforming growth factor-alpha (10 nM). Cyclosporin-A (5 microM) selectively inhibited cortisol-induced rises in the OTR concentration. The addition of cortisol to amnion cells increased OT-stimulated prostaglandin E2 (PGE2) release almost 100-fold; the combination of forskolin and cortisol increased the PGE2 response to OT about 5600 times. Judging from the greater effects on PGE2 release, these results suggest that forskolin and cortisol up-regulate the signal response mechanism to OT as well as the OTR concentration. The findings show that changes occurring in the amnion in vivo can be mimicked in vitro, and they elucidate the mechanism of up-regulation of OTR concentrations.
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PMID:Up-regulation of oxytocin receptors in rabbit amnion by glucocorticoids: potentiation by cyclic adenosine 3',5'-monophosphate. 840 89

The impact of insulin-like growth factor-I (IGF-I) basic fibroblast growth factor (bFGF), endothelin-1 (ET-1), tumour necrosis factor-alpha (TNF-alpha), transforming growth factor-alpha (TGF-alpha) and platelet-derived growth factor (PDGF) on the release of progesterone (P4) and oxytocin (OT) from individual bovine corpora lutea at different stages of the oestrous cycle and pregnancy was evaluated with a microdialysis system (MDS) in vitro. IGF-I (1 microgram mL-1) induced significantly the acute effects on P4 release at the late luteal stage (Days 15-18) and early pregnancy (Days 60-120), whereas bFGF (100 ng mL-1) was extremely effective in stimulating P4 release particularly during the mid-luteal stage (Days 8-12). Both peptides stimulated (P < 0.05) the release of OT throughout the three luteal stages and during early and late pregnancy (Days 30-60 and Days 150-210). ET-1 (100 ng mL-1) clearly inhibited P4 release during the early (Days 5-7) and mid-luteal phase and stimulated OT release only during the mid-luteal stage (P < 0.001). TNF-alpha (100 ng mL-1) stimulated the release of P4 exclusively at the early luteal phase (P < 0.05), whereas OT secretion was increased by TNF-alpha during all stages of the oestrous cycle (P < 0.001). TGF-alpha and PDGF (100 ng mL-1) were effective in stimulating P4 release particularly during late pregnancy (P < 0.05). In contrast, stimulation of OT secretion by TGF-alpha was maximal during the late-luteal stage (P < 0.001), whereas PDGF significantly increased OT secretion during the oestrous cycle (except the early luteal stage) and pregnancy (P < 0.001). The data demonstrate distinct and stage-specific effects of growth factors on P4 and OT secretion in vitro. IGF-I, bFGF and TGF-alpha may play an important role in corpus luteum (CL) function during the oestrous cycle and pregnancy since they are locally expressed and synthesized, there are receptors for these growth factors, and they have been demonstrated to exert biological effects on the CL.
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PMID:Effects of local growth factors on the secretory function of bovine corpus luteum during the oestrous cycle and pregnancy in vitro. 889 36