Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0406810 (NAME)
 13,345 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of this study was to determine whether nitric oxide (NO) mediates tumor necrosis factor (TNF)alpha influence on the bovine endometrium. TNFalpha influence on the bovine endometrium is limited to the stromal cells. Therefore, it was interesting to find out whether NO production by the stromal cells, stimulated by TNFalpha might influence the endometrial epithelium. Moreover, we investigated the intracellular mechanisms of TNFalpha- and NO-regulated prostaglandin (PG) F(2alpha) and PGE(2) synthesis. Epithelial and stromal cells from the bovine endometrium (Days 2-5 of the oestrous cycle) were separated by means of enzymatic dispersion and cultured for 6-7 days in 48-well plates. The confluent endometrial cells were exposed to a NO donor (S-NAP; 1-1000 microM) for 24 h. S-NAP strongly stimulated PGE(2) production in both bovine endometrial cell types (P<0.001). The effect of SNAP on PGF(2alpha) production was limited only to the stromal cells (P<0.05). To study the intracellular mechanisms of TNFalpha and NO action, stromal cells were incubated for 24 h with TNFalpha or S-NAP and with NO synthase (NOS) inhibitor (L-NAME; 10 microM) or an inhibitor of phosphodiesterase (IBMX; 10 microM). When the cells were exposed to TNFalpha in combination with NOS inhibitor (L-NAME), TNFalpha-stimulated PGs production was reduced (P<0.05). The inhibition of enzymatic degradation of cGMP by IBMX augmented the actions of S-NAP and TNFalpha on PGs production (P<0.05). The overall results suggest that TNFalpha augments PGs production by bovine endometrial stromal cells partially via induction of NOS with subsequent stimulation of NO-cGMP formation. NO also stimulates PGE(2) production in epithelial cells.
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PMID:Effects of nitric oxide and tumor necrosis factor-alpha on production of prostaglandin F2alpha and E2 in bovine endometrial cells. 1522 98

Electrical stimulation of sensory neurons that innervate receptors on the tailfan of crayfish evokes a reflex response of motor neurons that produce movements of the blades of the tailfan, the uropods. We analyzed the modulatory effects of nitric oxide (NO) on the spike frequency of the reflex response. Bath application of L-arginine and SNAP, which elevate endogenous and exogenous NO levels, increased the frequency of the evoked response, whereas the application of L-NAME and PTIO, which reduce NO levels, decreased the frequency of the response. To determine through what pathway and target NO exerted these effects we bath applied ODQ, an inhibitor of soluble guanylyl cyclase (sGC), which decreased the frequency of response, and 8-br-cGMP, which increased the spike frequency of response. To provide further evidence that NO acts via sGC, we elevated NO levels with L-arginine while simultaneously inhibiting sGC with ODQ. This application reduced the response to control levels, indicating that NO in the terminal ganglion of crayfish acts via sGC to modulate cGMP levels, which in turn regulate the responses of the uropod motor neurons.
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PMID:Nitric oxide modulates local reflexes of the tailfan of the crayfish. 1526 49

Recent studies have revealed a non-homogeneous distribution of nitric oxide synthase (NOS) in neurons. However, it is not yet clear whether the intracellular distribution of NOS represents the intracellular nitric oxide (NO) distribution. In the present study, software developed in our laboratory was applied to the reconstructed image obtained from confocal slice images in order to project the 3-D reconstructed images in any direction and to cut the neuron in different sections. This enabled the spatial distribution of NO to be visualized in any direction and section. In single neurons, NO distribution was seen to be heterogeneous. After stimulation with glutamate, the spatial changes in different areas of the neuron were different. These findings are consistent with immunocytochemical data on the intracellular localization of nNOS in hippocampus neurons, and will help to elucidate the specificity of nitric oxide signaling. Finally, the administration of SNAP and L-NAME was used to examine DAF-2 distribution in the neurons. The results showed this distribution to be homogenous; therefore, it did not account for the NO distribution results.
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PMID:Nitric oxide spatial distribution in single cultured hippocampus neurons: investigation by projection of reconstructed 3-D image and visualization technique. 1535 May 92

Angiogenesis is the process of new vessel formation from an existing vasculature network. In all but a few circumstances it is tightly controlled and suppressed. Precise understanding of the factors involved in modulation of angiogenesis has significant potential clinical value. One agent believed to play a role in angiogenesis is nitric oxide. However, there remain substantial uncertainties concerning the specifics of this role. The present study was undertaken to better define the role nitric oxide plays in angiogenesis associated with acute wound healing. Muscle biopsies from the pectoralis major of C57B6 mice were embedded in 500 microl of type I collagen matrix, and incubated in the presence of growth medium for 14 days. Treatment wells received L-Arginine (2 mM), L-NAME (300 microM), or SNAP (10-20 microM). Angiogenic response was quantified as the measure of cell migration through the matrix and as the total cells recovered from the matrix. Whole lung specimens and aortic segments served as sources of endothelial and vascular smooth muscle cells respectively for proliferation studies under similar treatment conditions. Nitric oxide was found to exert either a stimulatory or inhibitory effect on angiogenesis and cell proliferation that was subject to the assay system and specific vascular cell types present. These results suggest that the role of nitric oxide in angiogenesis is context dependent.
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PMID:Nitric oxide modulation of early angiogenesis. 1537 85

L-NAME-induced hypertension has been shown to produce concentric (eutrophic) remodeling of the heart despite an enhanced afterload. We postulated that nitric oxide synthase inhibition could limit coronary capillary growth to explain the nature of remodeling. To test our hypothesis, we aimed at determining the effect of endogenous and exogenous nitric oxide on coronary neovascularization. Aortic and coronary rings from normotensive animals were incubated in a three-dimensional type I collagen matrix in the presence of L-NAME or the nitric oxide donor SNAP. L-NAME inhibited, while SNAP stimulated, neovascularization from aortic and coronary rings after 12 days of in vitro incubation. In arterial rings harvested from rats treated with L-NAME for 14 days and in which no further in vitro treatment was added, only coronary rings showed a reduction in new capillary generation. While confirming that chronic L-NAME-treated rats develop concentric remodeling, the evaluation of capillary density did not reveal any difference as compared with the controls in 3 areas of the myocardium. In conclusion, chronic inhibition of nitric oxide synthesis in vivo produces a long-lasting reduction in the capacity of coronary arteries to generate new capillaries in vitro. Thus, our results lend support to the hypothesis that an inhibition of new capillary formation could prevent the development of compensatory ventricular hypertrophy, in favor of concentric remodeling.
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PMID:Chronic nitric oxide synthase inhibition prevents new coronary capillary generation. 1547 29

Excessive excitatory action of glutamate and nitric oxide (NO) has been implicated in degeneration of striatal neurons. Evidence had been provided that Na+K+-ATPase might be involved in this process. Here we investigated whether glutamate-regulated messengers, such as NO and cyclic GMP, could modulate the activity of membrane Na+K+-ATPase. Our results demonstrated that NO donors sodium nitroprusside (SNP at 30 and 300 microM) and S-nitroso-N-acetylpenicillamine (SNAP at 200 microM) increased alpha2,3Na+K+-ATPase activity which was blocked by the NO chelator, haemoglobin and was independent of [Na+]. This regulation was associated with cGMP synthesis and mimicked by glutamate (300 microM) and 8-Br-cyclic GMP (4 mM). 8-Br-cGMP-induced stimulation of Na+K+-ATPase activity could be blocked by KT5823 (an inhibitor of cGMP-dependent protein kinase, PKG), but not by KT5720 (an inhibitor of cAMP-dependent protein kinase, PKA). N-Methyl-D-aspartate (NMDA) receptors appeared to be involved in the effect of glutamate, since MK-801 (NMDA receptor antagonist) produced a partial reduction in glutamate-induced activation of the enzyme. MK-801 was not synergistic to L-NAME (NOS inhibitor), suggesting that glutamate stimulates the NMDA-NOS pathway to activate alpha2,3 Na+K+-ATPase in rat striatum. This regulation was associated with cyclic GMP (but not cyclic AMP) synthesis. These data indicate the existence, in vitro, of a regulatory pathway by which glutamate, acting through NO and cGMP, can cause alterations in striatal alpha2,3 Na+K+-ATPase activity.
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PMID:Glutamate modulates sodium-potassium-ATPase through cyclic GMP and cyclic GMP-dependent protein kinase in rat striatum. 1562 18

Evidence for the involvement of a bacterial nitric oxide synthase (NOS) in the biosynthesis of a phytotoxin is presented. Several species of Streptomyces bacteria produce secondary metabolites with unusual nitrogen groups, such as thaxtomin A (ThxA), which contains a nitroindole moiety. ThxA is a phytotoxin made by three pathogenic Streptomyces species that cause common scab of potato. All three species possess a gene homologous to the oxygenase domain of murine inducible NOS, and this gene, nos, is essential for normal levels of ThxA production. We grew Streptomyces turgidiscabies in the presence of several known NOS inhibitors and a nitric oxide (NO) scavenger to determine their effect on ThxA production. The NO scavenger (CPTIO) and four NOS inhibitors (NAME, NMMA, AG, and 7-NI) reduced ThxA production without affecting bacterial growth. A strain of S. turgidiscabies from which the nos gene had been deleted was grown in the presence of three NO donors (DEANO, SIN, and SNAP), and all three partially restored ThxA production. Our data suggest that bacterial nitric oxide synthases may, at least in part, produce NO for biosynthetic purposes, rather than for cellular signaling, as they do in mammals.
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PMID:Nitric oxide synthase inhibitors and nitric oxide donors modulate the biosynthesis of thaxtomin A, a nitrated phytotoxin produced by Streptomyces spp. 1563 47

During terminal differentiation of keratinocytes the expression of various proteins, which are required for the formation of the epidermal water barrier in the skin of land dwelling animals, is upregulated. Using a cell culture model for the differentiation of human keratinocytes and real-time PCR, we quantified the mRNA levels of several proteins involved in differentiation and ceramide metabolism. A calcium shift (1.1 mM CaCl2, 10 microM linoleic acid) for 8 days triggered an increase in mRNA levels of keratin 10 (75-fold), profilaggrin (55-fold), glucosylceramide synthase (40-fold), beta-glucocerebrosidase (30-fold), prosaposin (15-fold), acid sphingomyelinase (5-fold), and serine palmitoyltransferase (SPTLC2, 4-fold). However, mRNA levels of keratin 14 and acid ceramidase did not change significantly. On the other hand nitric oxide added at concentrations lower than 0.25mM stimulates proliferation of keratinocytes (Krischel et al., J. Invest. Dermatol. 111, 286-291, 1998). Accordingly, the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP, 0.2 mM) had no effect on the morphology of cultured keratinocytes, whereas in cultured human fibroblasts apoptosis was induced. The expression patterns obtained suggest that keratinocytes remain in a basal proliferative state, with a 3-fold increase in keratin 14 expression, a marked decrease in mRNA levels of differentiation markers and of most ceramide-metabolizing enzymes to negligible levels. The inhibitor of the NO synthase, N(G)-nitro-L-arginine-methyl ester (L-NAME, 10 mM), induced a transient increase in ceramide formation, followed by apoptosis in keratinocytes but not in fibroblasts. Both, SNAP and L-NAME, decreased the mRNA levels of all proteins involved in ceramide metabolism.
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PMID:Nitric oxide regulates synthesis of gene products involved in keratinocyte differentiation and ceramide metabolism. 1567 11

Matrix metalloproteinase (MMP) activity is upregulated in pathologies such as atherosclerosis during which endogenous nitric oxide (NO) biosynthesis is reduced. Diminished levels of NO, an antioxidant species, may result in higher oxidative stress. Oxidants are capable of activating MMPs from their zymogen forms. We examined whether basal biosynthesis of NO in the coronary circulation regulates MMP-2 activity. In isolated rat hearts perfused with Krebs-Henseleit buffer at a constant flow of 10 ml min(-1), we measured the release of MMP-2 into the coronary effluent by gelatin zymography. The main gelatinolytic activity of 72-kDa corresponds to MMP-2. Infusion of the NO synthase inhibitor N(G)-nitro-L-arginine methyl ester (L-NAME) concentration dependently increased coronary perfusion pressure (CPP) (by 48+/-11 mmHg with 100 microM) and enhanced the release of the 72-kDa MMP-2 in the effluent. Coinfusion of the NO donor S-nitroso-N-acetyl-D,L-penicillamine (SNAP, 1 microM) with L-NAME abolished both the increase in CPP and the enhanced MMP-2 release. The thromboxane A2 mimetic U46619 increased CPP to the same extent as L-NAME without increasing 72-kDa activity in the effluent, suggesting that MMP-2 release is not caused simply by enhanced perfusion pressure. Infusion of either L-NAME or U46619 did not significantly enhance LDH release. L-NAME infusion concentration dependently increased the level of lipid hydroperoxides in homogenates prepared from the perfused hearts. Coinfusion of SNAP prevented this increase. These data reveal another cytoprotective mechanism of endogenous NO biosynthesis in the heart, the inhibition of MMP-2 release.
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PMID:Inhibition of endogenous nitric oxide in the heart enhances matrix metalloproteinase-2 release. 1571 89

In mammals, the in vivo coronary blood flow and myocardial oxygen consumption are closely related via changes in coronary resistance in response to the metabolic demands of the myocardium. A fine neurohumoral regulation of coronary resistance holds true also in fish, and particularly in teleosts, where several vasoconstrictive and vasodilative mechanisms have been described, with numerous putative effectors, including prostanoids, acetylcholine, adrenaline, serotonin, adenosine, steroid hormones. Here, a resume is reported of the available evidence on the involvement of nitric oxide (NO) in the control of coronary resistance in teleosts and particularly in salmonids. Most of the evidence reported is from a comprehensive study performed on a Langedorff-type preparation of the isolated trout heart. Using a physio-pharmacological approach, the experiments performed on this preparation have demonstrated that trout coronary resistance is reduced by l-arginine (NOS substrate), nitroprusside and SNAP (NO donors) and is increased by the NOS inhibitors l-NNA and l-NAME. The vasodilation induced by nitroprusside is blocked by the guanylate cyclase inhibitor methylene blue. l-arginine increases NO release in the perfusate, while l-NNA reduces the release. NO release is inversely related with the coronary resistance. l-NNA inhibits the vasodilatory effects of acetylcholine, serotonin and adenosine. The vasodilation induced by adenosine is accompanied by NO release and involves stretch receptors. Hypoxia induces vasodilation and both adenosine and NO release in the preparation; the NO release under hypoxia is blocked by theophylline. On the whole these data indicate that NO plays a central role in the control of coronary resistance in trout. In particular, a main role for NO as an amplifier of the adenosine-mediated vasodilation under hypoxia can be hypothesized.
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PMID:Role of nitric oxide in the control of coronary resistance in teleosts. 1597 68


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