Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:4.1.1.17 (ornithine decarboxylase)
6,351 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Saponin, a naturally occurring plant glycoside, was found to elicit a prolactin-like stimulation of ornithine decarboxylase (ODC) activity in mouse mammary gland explants. A dose-response activation of ODC was observed with saponin at concentrations between 2 and 10 micrograms/ml. At concentrations of 10 and 15 micrograms/ml, saponin effected a response similar to that of PRL; when tested in concert, PRL and saponin caused a nonadditive response. The time-course of the saponin and PRL effects on ODC activation were not different; a maximum response occurred 2-4 hours after addition of saponin. The saponin and PRL responses were abolished by antibiotics (puromycin and cyclohexamide) that inhibit protein synthesis, but not by actinomycin D which inhibits RNA synthesis. Finally, saponin, by itself, did not affect the rate of milk product formation, but at higher concentrations (above 0.5 microgram/ml) impaired the PRL stimulation of lipid and casein synthesis.
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PMID:Saponin effects of prolactin-like stimulation of ornithine decarboxylase activity in mouse mammary gland explants. 147 13

Arthritis is produced in male rats within 9-10 days after a single injection of Freund's complete adjuvant (FCA) at the base of the tail. When bromocriptine, a dopaminomimetic that suppresses PRL secretion, was given in form of long-acting microcapsules (CBLA) 3 days before FCA, the hind limb swelling was significantly reduced by 70%. Here, we showed that plasma PRL levels were significantly elevated (by 150% over controls) during the 6-day period after FCA, particularly at night. Further, within 1-4 days after FCA inoculation, marked increases in ornithine decarboxylase (ODC) activity occurred in bone marrow, thymus, spleen, and lymph nodes (by 190%, 160%, 80% and 75% over control values, respectively). In FCA-treated rats, the circadian rhythm of thymic ODC showed that an important enhancement of activity occurred during the dark phase, which correlated with the peak of PRL secretion (between 2200-0400 h). Finally, pretreatment with CBLA significantly inhibited the induction of ODC in response to FCA in thymus, spleen, and lymph nodes (by 65%, 80%, and 45%, respectively) and inhibited it more weakly in the bone marrow. This in vivo study leaves little doubt about the existence of a PRL-dependent immuno-stimulatory mechanism, probably involved in the pathogenesis of adjuvant arthritis.
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PMID:Bromocriptine microcapsules inhibit ornithine decarboxylase activity induced by Freund's complete adjuvant in lymphoid tissues of male rats. 258 42

IGF-I stimulated the mitogenesis of Nb2 cells in the presence of suboptimal mitogenic concentrations of prolactin (PRL, 0.01 or 0.1 ng/ml). In the presence of 1 ng/ml or 10 ng/ml, concentrations of PRL that produced a maximal or near maximal mitogenic response in Nb2 cells, the addition of insulin-like growth factor-I (IGF-I) at 5 or 10 ng/ml did not further enhance mitogenesis. This effect was selective for IGF-I since IGF-II, epidermal growth factor (EGF), insulin, transforming growth factor-beta (TGF-beta) or platelet-derived growth factor (PDGF) did not stimulate mitogenesis in the presence or absence of PRL. That the ability of IGF-I to stimulate mitogenesis of these cells required PRL was suggested by the ability of PRL antiserum to block the IGF-I effect. Monoclonal antibody to IGF-I reduced the mitogenic response to one identical to PRL alone. In the presence of a suboptimal mitogenic concentration of PRL, IGF-I was an equally effective comitogen when added at 0 time or at 6 h after PRL stimulation, suggestive of an effect of IGF-I in late G1 phase of the cell cycle. Effects of IGF-I on ornithine decarboxylase, a G1 enzymatic marker, were compatible with this interpretation. In order to be assured that IGF-I exerted its action through a receptor-mediated process, we evaluated the presence of IGF-I receptors on Nb2 cells. Receptors were present which bound IGF-I greater than IGF-II much greater than insulin. The IC50 was 35 nM for IGF-I, 280 nM for IGF-II and 875 nM for insulin.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Enhancement of prolactin (PRL)-stimulated mitogenesis of Nb2 rat lymphoma cell cultures by insulin-like growth factor I (IGF-I). 277 31

The effect of daily treatment with the pure antiandrogen Flutamide has been studied either alone or in combination with the LHRH agonist [D-Trp6, des-Gly-NH2(10)]LHRH ethylamide (LHRH-A), on testicular and prostatic functions in adult male rats. Treatment for 10 days with Flutamide (5 mg/rat, twice daily) caused a marked stimulation of plasma testosterone (T) associated with a significant increase in plasma gonadotropin concentrations and inhibited plasma PRL levels. Testicular weight is not changed following antiandrogen administration but testicular LH/hCG receptor levels are markedly decreased with no change in FSH receptor levels. Moreover, Flutamide treatment alone produces an important inhibition of ventral prostate and seminal vesicle weights associated with a significant decrease in prostatic beta-adrenergic receptor levels but no change is observed in specific ornithine decarboxylase (ODC) activity. Daily LHRH-A treatment at the dose of 1 microgram/day for 10 days decreases plasma T to levels comparable to those found in orchiectomized men (0.30 +/- 0.5 ng/ml). This effect is associated with an almost complete loss of testicular LH/hCG receptors, a decrease in testicular weight, a significant increase in plasma gonadotropins and a marked inhibition of plasma PRL concentration. A relatively smaller inhibition of ventral prostate and seminal vesicle weights follows treatment with the LHRH agonist alone, this effect being accompanied by a significant reduction in beta-adrenergic receptor concentration but no change in prostatic ODC activity. Combination of the two drugs, however, caused a potent inhibitory effect on both ventral prostate and seminal vesicle weight to values similar to those found in castrated rats. The prostatic weight loss is accompanied by a marked fall in ODC activity and in the concentration of beta-adrenergic receptors. The present data clearly show that combined treatment with an LHRH agonist and a pure antiandrogen is highly effective in inhibiting, not only prostatic growth, but also two androgen-sensitive parameters of prostatic activity.
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PMID:Characteristics of flutamide action on prostatic and testicular functions in the rat. 283 89

The activity of S-adenosylmethionine decarboxylase (SAM-DC) has been measured in the adrenal gland of rats given treatments that are known to result in increased activity of ornithine decarboxylase in this organ. In contrast to the effects of the dopamine agonists piribedil and apomorphine on the latter enzyme, the administration of these drugs caused decreases of SAM-DC in both parts of the gland. After piribedil the activity decreased rapidly to a minimum at 2-4 h, with recovery by 6 h. The stress of immobilization or the administration of insulin or 2-deoxyglucose (2-DG) also decreased adrenal SAM-DC activity. The results contrast with those observed in other rat tissues where SAM-DC is generally induced by treatments that induce ornithine decarboxylase. Denervation of the adrenal gland did not clearly affect the reduction in adrenomedullary SAM-DC after 2-DG. Hypophysectomy resulted in reduced SAM-DC activity in both adrenal medulla and cortex; the activity could be restored by giving the animals 2 IU ACTH daily for 4 days. These changes in activity were parallelled by changes in immunoreactive protein. 2-DG did not decrease SAM-DC in hypophysectomized rats receiving maintenance ACTH dosage. This indicates the presence of hormonal control over the activity of SAM-DC in the adrenal medulla and cortex. Acute administration of an additional 10 IU ACTH to hypophysectomized rats on maintenance dosage of ACTH resulted in decreased SAM-DC activity in both adrenal medulla and cortex. These decreases were not abolished by inhibition of corticosteroid synthesis with metopirone. PRL and GH had no significant effect on adrenal SAM-DC activity of hypophysectomized rats. The reduction of SAM-DC activity in both parts of the gland of hypophysectomized rats with administration of (Bu)2cAMP suggests that cAMP may mediate the decreases in SAM-DC caused by the above treatments.
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PMID:Decreased activity of adrenal S-adenosylmethionine decarboxylase in rats subjected to dopamine agonists, metabolic stress, or bodily immobilization. 303 Jun 95

The circadian time of PRL administration is an important determinant of its stimulatory activity in pigeon crop tissue. Based on previously published experiments we chose two phases of the entrained circadian cycle (0 and 9 h after light onset) which represent minimum and maximum crop sensitivity and examined several specific biochemical markers of mitogenesis and differentiation. These included DNA synthesis, ornithine decarboxylase activity, total RNA concentration, polyadenylated RNA concentration, and a specific PRL-induced messenger RNA. In confirmation of previous studies, crop weight was increased twice as much by ovine PRL (0.5 micrograms/g BW X 3 days) injected 9 h after light onset compared with the 0 h time of injection. A single local injection of 10 micrograms of ovine-PRL increased DNA synthesis by 4-fold when injection was made at 9 h but had no effect when injection was made at 0 h after light onset. In contrast, PRL stimulation of gene expression, including total RNA, polyadenylated RNA, and a specific PRL-induced messenger RNA, were quantitatively identical at each phase of the circadian cycle. Corollary with its central role in cell proliferation, ornithine decarboxylase activity was induced by PRL injected at 9 h after light onset. The mitogenic and differentiational PRL effects in crop are therefore partially dissociable and may depend on distinct mechanisms.
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PMID:The mitogenic, but not differentiative, response of crop tissue to prolactin is circadian phase dependent. 398 31

The actions of PRL on RNA and casein synthesis were tested in mouse mammary gland explants that were cultured with medium containing several concentrations of calcium ions. The PRL effects on both RNA and casein synthesis were the same when calcium concentrations between 0.3-11.3 mM were employed. In the absence of extracellular calcium ions, however, PRL had no action on RNA or casein synthesis, but a significant stimulation of ornithine decarboxylase activity by PRL was observed in the absence of calcium. Stimulatory actions of insulin, cGMP, and prostaglandin F2 alpha on RNA synthesis in the cultured explants were observed in the absence of calcium, but arachidonic acid had no effect under these conditions. It is concluded that specific actions of PRL in the mammary gland require the presence of extracellular calcium ions.
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PMID:Calcium requirement for prolactin actions on ribonucleic acid and casein synthesis in mouse mammary gland explants. 615 71

Phospholipases A2 (PLA2) and C (PLC) stimulate ornithine decarboxylase (ODC) activity in mouse mammary gland explants preincubated with insulin and cortisol. PLC concentrations of 0.1 micrograms/ml produced responses that were close in magnitude to that of PRL, whereas PLA2 at concentrations of 5-50 micrograms/ml was 35-40% as efficacious as 1 microgram/ml PRL in stimulating ODC activity. The time courses of PLC, PLA2, and PRL actions on ODC activity were not different from one another. When PRL and PLC were tested together, a response greater than the sum of the responses of each of these agents alone was observed; PLA2 (25 micrograms/ml) when tested with PRL produced a nonadditive response. The action of PRL on ODC activity was significantly attenuated by quinacrine, an inhibitor of PLC and PLA2 activities. These results suggest that PRL, PLA2, and PLC stimulate ODC activity via similar mechanisms in the mammary gland and make tenable the idea that the action of PRL on ODC activity may be carried out via an action of PRL on PL activity.
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PMID:Effects of phospholipases on ornithine decarboxylase activity in mammary gland explants from midpregnant mice. 664 23

PRL has been shown to induce a number of genes after the stimulation of quiescent Nb2 T-cells, including c-fos, c-myc, ornithine decarboxylase, interferon regulatory factor-1, and others. One of these genes, LHRH, has not previously been reported to respond in this manner, although we and others have reported its presence in rat and human T- and B-cells. Furthermore, recent evidence suggests that LHRH functions as an immunoregulator in a cytokine-like manner. Using the rat immature T-cell line Nb2, we present data showing for the first time that 1) the LHRH gene is regulated by PRL at various times during the cell cycle; 2) an alternatively spliced LHRH messenger RNA exists in Nb2 cells and may produce a new truncated GnRH-associated peptide (alternatively called PIF for PRL-inhibiting factor); 3) the LHRH receptor is expressed in lymphocytes in a manner similar to the LHRH gene after PRL addition, and its complementary DNA sequence is identical to that of the pituitary receptor; 5) the SH gene, found on the opposite strand of the LHRH gene, is expressed in lymphocytes at the same time and in the same manner as the LHRH gene; 6) the LHRH messenger RNA has a very short half-life in these cells; and 7) the lymphocyte LHRH transcription start site is essentially the same as the hypothalamic site. These data strengthen the relationship between PRL and LHRH expression in the immune system and further support our contention that LHRH is an important immunoregulator, on par with other known cytokines.
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PMID:Coordinate gene expression of luteinizing hormone-releasing hormone (LHRH) and the LHRH-receptor after prolactin stimulation in the rat Nb2 T-cell line: implications for a role in immunomodulation and cell cycle gene expression. 776 Aug 50

Human prolactin (hPRL) induced ornithine decarboxylase (ODC) activity, subsequently DNA synthesis and cellular proliferation on human promyelocytic cells, HL60, cultured in a serum-free medium. HL60 cells had 2100 specific binding sites for hPRL per cell, showing a dissociation constant of 1.1 x 10(-10) M. Binding of 125I-PRL to the cells was not blocked by simultaneous addition of human growth hormone. ODC activity and DNA synthesis were activated maximally at 5 and 20 h, respectively, after the addition of 0.05 nM hPRL. These effects of PRL on cellular proliferation, ODC activity and DNA synthesis were abolished by the simultaneous addition of anti-hPRL antibody. Simultaneous addition of an irreversible inhibitor of ODC, difluoromethyl ornithine (DFMO), also abolished the inductions of ODC and DNA synthesis by hPRL. The inhibitory effect of DFMO on hPRL-induced DNA synthesis was reversed by the addition of putrescine to the culture medium. These results suggest that hPRL binds to the prolactin receptor on HL60 cells and induces ODC activity to increase cellular polyamine levels, which eventually stimulates DNA synthesis and cellular proliferation.
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PMID:Human promyelocytic cell line HL60 has the specific binding sites for prolactin and its ornithine decarboxylase, DNA synthesis and cellular proliferation are induced by prolactin. 835 6


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