Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.6.1.3 (ATPase)
65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The acute effect of intraperitoneally administered prolactin (0.2, 0.4, and 0.6 mg/kg body weight) on passive calcium transport in duodenum, proximal jejunum, and ileum of sexually mature female Wistar rats was investigated by using an in vivo perfusion technique. Test solution containing (in mM) NaCl, 100; KCl, 4.7; MgSO4, 1.2; CaCl2, 20; D-glucose, 11; sodium ferrocyanide (Na4Fe(CN)6), an index of net water transport, 20; and 0.7 microCi 45CaCl2 (1 Ci = 37 GBq) was perfused through the 10-cm intestinal loop for 60 min. Results showed that 0.4 mg prolactin/kg body weight significantly increased duodenal net Ca absorption (net Ca) from 23.81 +/- 1.84 to 30.56 +/- 1.57 mmol/g dry weight (p < 0.05) by stimulating the lumen to plasma calcium flux (CaL-P). The jejunum responded to 0.2, 0.4, and 0.6 mg prolactin/kg body weight by reversing from net Ca absorption of 18.60 +/- 1.70 mmol/g dry weight to net secretion of -3.30 +/- 1.56, -10.39 +/- 2.21, and -11.79 +/- 2.04 mmol/g dry weight (p < 0.01), respectively, as a result of a dose-dependent increase in plasma to lumen calcium flux (CaP-L). Calcium fluxes in the ileum on the other hand did not respond to prolactin. There was a close correlation between net water flux and net calcium flux in all three intestinal segments under basal condition regardless of the luminal sodium concentration. However, this correlation was lost after prolactin administration, which while having no effect on net water flux, altered the duodenal and jejunal calcium fluxes. By varying the luminal concentration of sodium, it was found that the stimulatory effect of 0.4 mg prolactin/kg body weight on the duodenal CaL-P was reduced when compared with control, i.e., 17.84 +/- 0.91 vs. 26.64 +/- 1.05 mmol/g dry weight at a sodium concentration of 180 mM, and 14.48 +/- 0.99 vs. 20.12 +/- 1.34 mmol/g dry weight at a sodium concentration of 140 mM. At a sodium concentration of 80 mM, the prolactin effect was absent. Since duodenal Na(+)-K+ ATPase activity was increased by prolactin from 3.77 +/- 0.16 to 4.95 +/- 0.30 mumol Pi.mg-1 protein.h-1 (p < 0.05), sodium dependency of the prolactin-enhanced lumen to plasma calcium flux may be related to both sodium-induced water flow and calcium-sodium exchange across the basolateral membrane. Thus, it was postulated that under basal condition, net calcium transport in the small intestine occurred with the sodium-induced water transport along the paracellular pathway. However, after prolactin administration, this association was lost. Prolactin-enhanced lumen to plasma calcium flux in the duodenum was sodium dependent and involved the Na(+)-K+ ATPase activity. In the proximal jejunum, prolactin stimulated plasma to lumen calcium flux, but the mechanism was not known.
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PMID:Acute effects of prolactin on passive calcium absorption in the small intestine by in vivo perfusion technique. 963 55

The potential effects of growth hormone (GH), prolactin (Prl), and triiodothyronine (T3) on gill Na+,K+-ATPase activity and corticosteroid receptor (CR) concentration (Bmax) and dissociation constant (Kd) were examined in juvenile Atlantic salmon (Salmo salar). Compared to controls, fish injected with GH (ovine, 5.0 microgram g-1) had significantly greater gill Na+,K+-ATPase activity after 7 and 14 days. Gill CR Bmax and Kd were significantly elevated on day 7, but not day 14. T3 also significantly increased CR Bmax. The effect of GH on CR Bmax was also additive with T3 (5.0 microgram g-1) treatment. There was a synergistic effect on CR Bmax when purified coho salmon GH (csGH, 0.1 microgram g-1) was injected in combination with T3 (1.6 microgram g-1). Prl (ovine, 5.0 microgram g-1; purified coho salmon, 0.1 microgram g-1) did not significantly alter gill CR Bmax. Although Prl limited the increase in CR Bmax by GH, the effect was not signicant. T3 and Prl did not have an effect on Kd. GH significantly increased gill Na+,K+-ATPase activity, T3 administration did not have a significant effect, and Prl-treated fish had significantly lower gill Na+,K+-ATPase activity. The results indicate that T3 acts additively with GH, while Prl has no effect in regulating CR Bmax. An increase in cytosolic CR by GH and T3, but not Prl, may regulate gill responsiveness to cortisol and be an important mechanism in the endocrine control of physiological changes during the parr-smolt transformation.
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PMID:Regulation of gill cytosolic corticosteroid receptors in juvenile Atlantic salmon: interaction effects of growth hormone with prolactin and triiodothyronine. 978 10

Lithium is used in the prophylaxis of bipolar depressive disorder in augmentation treatment of depression and in the therapy of some cases of unipolar depression. Lithium affects cell function via its inhibitory action on adenosine triphosphatase (ATPase) activity, cyclic adenosine monophosphate (cAMP), and intracellular enzymes. The inhibitory effect of lithium on inositol phospholipid metabolism affects signal transduction and may account for part of the action of the cation in manic depression. Lithium also alters the in vitro response of cultured cells to thyrotropin-releasing hormone (TRH) and can stimulate DNA synthesis. Lithium is concentrated by the thyroid and inhibits thyroidal iodine uptake. It also inhibits iodotyrosine coupling, alters thyroglobulin structure, and inhibits thyroid hormone secretion. The latter effect is critical to the development of hypothyroidism and goiter. Effects on brain deiodinase enzymes and alterations in thyroid hormone receptor concentration in the hypothalamus are under investigation in relation to the therapeutic effect of lithium. The ion affects many aspects of cellular and humoral immunity in vitro and in vivo. This accounts for a rise in antithyroid antibody titer in patients having these antibodies before lithium administration whereas there is no induction of thyroid antibody synthesis de novo. Goiter, due to increased thyrotropin (TSH) after inhibition of thyroid hormone release, occurs at various reported incidence rates from 0%-60% and is smooth and nontender. Subclinical and clinical hypothyroidism due to lithium is usually associated with circulating anti-thyroid peroxidase (TPO) antibodies but may occur in their absence. Iodine exposure, dietary goitrogens, and immunogenetic background may all contribute to the occurrence of goiter and hypothyroidism during long-term lithium therapy. It is currently unclear whether the reported association of lithium therapy and hyperthyroidism are causal, although there is suggestive epidemiological evidence. Finally, lithium therapy is associated with exaggerated response of both TSH and prolactin to TRH in 50%-100% of patients, although basal levels are not usually high. It is probable that the hypothalamic pituitary axis adjusts to a new setting in patients receiving lithium.
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PMID:The effects of lithium therapy on thyroid and thyrotropin-releasing hormone. 982 58

Silver seabream (Sparus sarba) held in seawater (33 per thousand) or acclimated to a hypoosmotic environment of 6 per thousand were given intraperitoneal injections of saline (0.8% NaCl), recombinant bream growth hormone (rbGH, 1 microg/g), or ovine prolactin (oPRL, 6microg/g) for 7 consecutive days. Serum Na+ levels were unaffected by hypoosmotic acclimation and rbGH and oPRL treatment. Treatment of seawater fish with oPRL resulted in hyperchloremia. In 6 per thousand, saline-treated fish exhibited elevated branchial chloride cell (CC) numbers and exposure indices, all of which were markedly reduced by oPRL. CC numbers and morphometrics were unaffected by oPRL in seawater fish. In contrast, rbGH treatment of seawater fish resulted in elevated CC numbers, apical area, and fractional area and, in 6 per thousand fish, elevated CC fractional area and exposure numbers. Branchial Na+-K+-ATPase activity reduced in saline-treated fish adapted to 6% but was unaffected by rbGH regardless of salinity. oPRL reduced activity in both seawater and 6 per thousand-adapted fish. Neither hypoosmotic adaptation nor oPRL had any effect on renal Na+-K+-ATPase activity whereas rbGH reduced activity in both 33 and 6 per thousand. Saline-treated fish adapted to 6 per thousand exhibited reduced Na+-K+-ATPase activity in most regions of the intestine. Treatment with rbGH did not change intestinal Na+-K+-ATPase activity of seawater fish but elevated activity in the anterior regions (esophagus and stomach) of 6 per thousand-adapted fish. Treatment with oPRL elevated Na+-K+-ATPase activity throughout the gastrointestinal tract of seawater fish and in the anterior reaches of 6 per thousand-adapted fish. The data indicated that the as yet uncharacterized osmoregulatory roles of PRL and GH in seabream may warrant further attention as the present study connoted differing responses to that of other teleosts studied.
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PMID:Effects of prolactin and growth hormone on strategies of hypoosmotic adaptation in a marine teleost, Sparus sarba. 988 39

The effect of hormone treatment on the abundance of Na+-K+-ATPase alpha- and beta-subunit mRNA in Sparus sarba branchial tissue was investigated. Groups of seawater (33/1000) and hypo-osmotic (6/1000) acclimated fish were injected daily, with either saline, cortisol, recombinant bream growth hormone (rbGH) or ovine prolactin (oPRL). Total RNA from branchial tissue was analyzed by Northern blotting using PCR amplified Na+-K+-ATPase alpha- and beta-subunit cDNA clones. Na+-K+-ATPase alpha- and beta- subunit transcripts of 3.3kb and 2.4kb respectively, were detected and their abundance, after hormone treatment was assessed using RNA dot blots. The abundance of subunit mRNAs increased 1.4-1.9 fold, relative to controls, after cortisol treatment. The alpha:beta mRNA ratio also increased in cortisol treated seawater acclimated fish. Growth hormone treatment did not cause any significant changes in Na+-K+-ATPase subunit mRNA, whereas prolactin significantly reduced alpha-subunit mRNA levels by approximately 0.5 fold in both seawater and hypo-osmotic conditions. The data from this study add further support to the generally accepted roles that cortisol and prolactin have in the modulation of Na+-K+-ATPase activity. It can be concluded from this study that S. sarba branchial Na+-K+-ATPase subunit expression is multihormonally regulated.
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PMID:Hormonal modulation of branchial Na+-K+-ATPase subunit mRNA in a marine teleost Sparus sarba. 1035 Mar 56

A 2-factorial (3x3) injection experiment was used to investigate the effect and interaction between different hormones on the initial phase of seawater (SW) acclimation in brown trout (Salmo trutta). Each fish was given 4 injections on alternate days in freshwater (FW). Factor 1 was either saline, 2 micrograms ovine prolactin (oPRL)/g, or 2 micrograms ovine growth hormone (oGH)/g. Factor 2 was either 0, 0. 01, or 0.1 mirograms recombinant human insulin-like growth factor-I (rhIGF-I)/g. In each of the 9 treatment groups, half of the fish were subjected to a 48-h SW-challenge test, and the remaining fish were sham-transferred to FW one day after the last injection. Hypo-osmoregulatory performance was increased by GH and impaired by PRL treatment as judged by changes in plasma osmolality, [Na+], [Cl-], total [Mg] and muscle water content (MWC) after SW transfer. IGF-I reduced plasma osmolality after transfer to SW but had no effect on plasma total [Mg] or MWC. The effects of the two factors on plasma osmolality, [Na+], [Cl-], and MWC were additive. In sham-transferred fish, GH and IGF-I, alone and in combination, stimulated Na+,K+-ATPase alpha-subunit mRNA (alpha-mRNA) content in the gill. This was paralleled by an overall increase in gill Na+, K+-ATPase activity in fish treated with 0.01 micrograms IGF-I/g. Simultaneous administration of PRL completely inhibited the increase in gill alpha-mRNA observed in the IGF-I-injected groups. Combination of GH and IGF-I did not further affect the alpha-mRNA level relative to the single hormone-injected groups. There was an overall decrease in Na+,K+-ATPase activity in pyloric caeca and middle intestine by the low dose and both doses of IGF-I respectively. No effect was observed in the posterior intestine. PRL and GH treatments did not affect enzyme activity in any intestinal segment. Both doses of IGF-I increased Na+,K+-ATPase-immunoreactive (NKIR) cell density in gill primary filaments. PRL and GH had no effect on primary filament NKIR cell density. GH and both doses of IGF-I reduced secondary lamellar NKIR cell density, whereas PRL had no effect. The main conclusion is that IGF-I and GH induce an overall redistribution of NKIR cells away from the secondary lamella onto the primary filament of FWacclimated trout. This is associated with an overall increased alpha-mRNA level in the gill, which may reflect an increased expression within individual NKIR cells in the primary filament. PRL completely abolished the IGF-I stimulation of alpha-mRNA levels, suggesting a desensitisation of the gill tissue to IGF-I, which may explain the overall anti-SW adaptive effect of PRL.
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PMID:Endocrine control of Na+,K+-ATPase and chloride cell development in brown trout (Salmo trutta): interaction of insulin-like growth factor-I with prolactin and growth hormone. 1039 29

Prolactin enhances progesterone-dependent transcription of the rabbit uteroglobin gene. RUSH transcription factors are implicated in the signal transduction pathway. The RUSH acronym identifies key features of these nuclear phosphoproteins, that is, RING-finger motif, binds the uteroglobin promoter, structurally related to the SWI/SNF family of transcription factors, and helicase-like. Cloned by recognition site screening, RUSH proteins bind to an 85-bp region (-170/-85) of the uteroglobin promoter that was subsequently identified as a novel prolactin-responsive region by promoter deletion analysis. Gel shift and linker-scanning assays further reduced the RUSH target site to -160/-110. A hexameric core of MCWTDK was identified as the RUSH-specific DNA-binding site (-126/-121) by CASTing. This site overlaps authentic HNF3 beta and OCT-1 binding sites. A unique Type IV P-type ATPase that is embedded in the inner nuclear membrane binds the RING domain of RUSH. The conformationally flexible loop portion of this RING-finger binding protein (RFBP) extends into the nucleoplasm to contact euchromatin. The physical association of RFBP with transcriptionally active chromatin supports the speculation that RFBP targets RUSH transcription factors to the active uteroglobin promoter.
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PMID:Uteroglobin gene transcription: what's the RUSH? 1119 55

It is well established that prolactin (PRL) sustains, while prostaglandin F(2 alpha) (PGF(2 alpha)) curtails, progesterone production by the rat corpus luteum (CL). We have previously shown that the actions of both molecules converge on the 20 alpha-HSD gene and control its expression in a dramatically opposed manner. In this investigation, we have found twelve more genes that are inversely regulated by PRL and PGF(2 alpha). In addition to 20 alpha-HSD, PGF(2 alpha) stimulated and PRL inhibited PGF(2 alpha)-receptor, phospholipase C delta(1) and TGF beta(1) expression. In contrast PRL stimulated and PGF(2 alpha) inhibited the LH receptor, 11 beta-HSD2, sterol carrier protein 2, mitochondrial glutathione S-transferase (GST), GST mu(2), inhibitory DNA-binding proteins 1, 2, and 3, and calcium binding protein 2. We have also identified new target genes for PRL and PGF(2 alpha). PGF(2 alpha) stimulated the expression of genes involved in cell signaling such as cell adhesion kinase-beta, ERK3, FRA2, IL-2 receptor, and 14-3-3 proteins. PGF(2 alpha) also up-regulated the expression of the sodium channel beta(1), Na/K ATPase, annexin IV, GST7pi, and P450 reductase. In contrast PGF(2 alpha) inhibited the expression of two genes involved in cell cycle: cyclin D2 and retinoblastoma related protein (Rb2/p130). It also inhibited genes involved in estradiol (P-450(AROM)) and cholesterol biosynthesis (HMG-CoA synthase), as well as genes involved in tissue remodeling: VEGF and TIMP3. PRL had a profound inhibitory effect on the expression of genes encoding the ADP-ribosylation factor 3, annexin V and c-jun, yet increased the expression of P450scc, 3beta-HSD, and SR-B1 (HDL-receptor), all genes involved in steroidogenesis. PRL also stimulated the expression of beta(2)-microglobulin, TIMP2, cytochrome c oxidase IV, cathepsin H and L, and copper-zinc superoxide dismutase as well as elongation factor SIII, heat shock protein-60 and mitochondrial ATP synthase-D. In conclusion, this investigation has revealed a "yin-yang" relationship between PRL and PGF(2 alpha) in regulating certain critical genes in the rodent CL, and has demonstrated novel regulation by these factors of other important genes involved in luteal function.
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PMID:Opposite effect of prolactin and prostaglandin F(2 alpha) on the expression of luteal genes as revealed by rat cDNA expression array. 1151 96

The physiological effects of ovine prolactin (oPRL) and recombinant rainbow trout prolactin (rbtPRL) on cultured gill epithelia derived from freshwater rainbow trout were assessed. Epithelia composed of either pavement cells only (single seeded inserts, SSI) or both pavement and mitochondria-rich cells (double seeded inserts, DSI) were cultured in media, supplemented with doses of oPRL ranging from 10 to 100 ng/ml. Under symmetrical culture conditions (L15 media apical/L15 media basolateral), oPRL had no effect on transepithelial resistance, paracellular permeability (assessed with PEG-4000), or Na(+) and Cl(-) transport across both preparations of cultured gill epithelia. Under asymmetrical conditions (freshwater apical/L15 media basolateral), SSI epithelia treated with oPRL (10 and 50 ng/ml), in comparison to comparably treated epithelia receiving no oPRL, exhibited a greater increase in the transepithelial resistance, particularly during the first 12h of freshwater exposure, no difference in paracellular permeability and Na(+)-K(+)-ATPase activity, and lowered net Na(+) flux rates (i.e., reduced basolateral to apical loss rates). These reflected reduced unidirectional efflux rates. The PRL effect appeared to be mainly a reduction in transcellular permeability. SSI epithelia treated with rbtPRL (10 ng/ml) exhibited similar patterns of response to those treated with oPRL. Na(+)-K(+)-ATPase activity increased in DSI epithelia treated with oPRL; however, oPRL did not stimulate ion uptake across either SSI or DSI epithelial preparations. The data demonstrated that, as the sole hormone supplement for cultured gill epithelia, PRL did not promote active ion uptake. However, the observed PRL-induced alterations in cultured gill epithelial physiology were consistent with the in vivo actions of PRL on the gills of freshwater teleost fish.
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PMID:Prolactin effects on cultured pavement cell epithelia and pavement cell plus mitochondria-rich cell epithelia from freshwater rainbow trout gills. 1227 Jul 87

We review recent progress in the development of models for the freshwater teleost gill based on reconstructed flat epithelia grown on permeable filter supports in primary culture. Methods are available for single-seeded insert (SSI) preparations consisting of pavement cells (PVCs) only from trout and tilapia, and double-seeded insert (DSI) preparations from trout, containing both PVCs (85%) and mitochondria-rich cells (MRCs, 15%), as in the intact gill. While there are some quantitative differences, both SSI and DSI epithelia manifest electrical and passive permeability characteristics typical of intact gills and representative of very tight epithelia. Both preparations withstand apical freshwater exposure, exhibiting large increases in transepithelial resistance (TER), negative transepithelial potential (TEP), and low rates of ion loss, but there is only a small active apical-to-basolateral "influx" of Cl(-) (and not of Na(+)). Responses to various hormonal treatments are described (thyroid hormone T3, prolactin, and cortisol). Cortisol has the most marked effects, stimulating Na(+),K(+)-ATPase activity and promoting active Na(+) and Cl(-) influxes in DSI preparations, and raising TER and reducing passive ion effluxes in both epithelia via reductions in paracellular permeability. Experiments using DSI epithelia lacking Na(+) uptake demonstrate that both NH(3) and NH(4)(+) diffusion occur, but are not large enough to account for normal rates of branchial ammonia excretion, suggesting that Na(+)-linked carrier-mediated processes are important for ammonia excretion in vivo. Future research goals are suggested.
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PMID:Cultured gill epithelia as models for the freshwater fish gill. 1242 39


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