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:1.5.1.19 (NOS)
7,285 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mucocele-like tumor and invasive mucinous carcinoma of the breast may represent the two ends of the pathological spectrum of mucinous lesions of the breast, respectively. Little data exists on mucinous lesions that may be considered intermediate between mucocele-like tumor and invasive mucinous carcinoma. We studied 23 consecutive cases of invasive mucinous carcinoma of the breast and observed the following associated intermediate mucinous lesions: mucin-filled ducts (MFD) with unremarkable epithelium in 15 cases (65%), MFD with typical ductal hyperplasia in 9 cases (39%), MFD with atypical ductal hyperplasia in 5 cases (22%), and MFD with intraductal carcinoma in 13 cases (57%; micropapillary or cribriform types). Eighteen cases (78%) contained MFD with one of these four lesions and five cases (22%) contained all four lesions. Twenty-three consecutive cases of infiltrating ductal carcinoma-not otherwise specified (IDC-NOS), 21 cases of intraductal carcinoma, and 50 consecutive cases of surgically-excised breast tissue with fibrocystic change (FC), were similarly reviewed. Only one case (4%) of IDC-NOS, 1 case of intraductal carcinoma, and two cases (4%) of FC, contained small foci of MFD with intraductal carcinoma, intraductal carcinoma, and unremarkable epithelium, respectively. Our findings suggest the presence of a spectrum of mucinous lesions of the breast which represents a pathological continuum.
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PMID:Mucinous lesions of the breast. A pathological continuum. 830 9

Six gene markers have been used to map the progress of the innate immune response of the mosquito vector, Anopheles gambiae, upon infection by the malaria parasite, Plasmodium berghei. In addition to four previously reported genes, the set of markers included NOS (a nitric oxide synthase gene fragment) and ICHIT (a gene encoding two putative chitin-binding domains separated by a polythreonine-rich mucin region). In the midgut, a robust response occurs at 24 h post-infection, at a time when malaria ookinetes traverse the midgut epithelium, but subsides at later phases of malaria development. In contrast, the salivary glands show no significant response at 24 h, but are activated in a prolonged late phase when sporozoites are released from the midgut into the haemolymph and invade the glands, between 10 and 25 days after blood feeding. Furthermore, the abdomen of the mosquito minus the midgut shows significant activation of immune markers, with complex kinetics that are distinct from those of both midgut and salivary glands. The parasite evidently elicits immune responses in multiple tissues of the mosquito, two of which are epithelia that the parasite must traverse to complete its development. The mechanisms of these responses and their significance for malaria transmission are discussed.
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PMID:Malaria infection of the mosquito Anopheles gambiae activates immune-responsive genes during critical transition stages of the parasite life cycle. 979 21

Porphyromonas gingivalis is a Gram-negative periodontopathic bacterium colonizing the oral cavity and its lipopolysaccharide (LPS) is a key factor in the development of periodontitis. We investigated the effect of P. gingivalis LPS on the cellular responses associated with mucin synthesis in sublingual salivary gland acinar cells. Exposure of the acinar cells to the LPS led to a dose-dependent decrease in mucin synthesis and was accompanied by a massive induction in inducible nitric oxide synthase (NOS-2) activity and the increase in NO production, caspase-3 activity and apoptosis. Inhibition of extracellular signal-regulated kinase (ERK) with PD98059 accelerated the LPS-induced decrease in the glycoprotein synthesis and caused further increase in apoptosis and NOS-2 activity, while the blockade of p38 mitogen-activated kinase (MAPK) with SB203580 countered the LPS-induced reduction in the glycoprotein synthesis and obviated the induced increases in NOS-2 and apoptosis. Introduction of NOS-2 inhibitor, L-NAME, not only countered the LPS-induced increase in NO generation, caspase-3 activity and apoptosis, but caused the impedance of the LPS inhibition on mucin synthesis. The findings point to the upregulation in NOS-2 expression by P. gingivalis LPS as a key detrimental culprit affecting salivary mucin synthesis.
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PMID:Porphyromonas gingivalis lipopolysaccharide interferes with salivary mucin synthesis through inducible nitric oxide synthase activation by ERK and p38 kinase. 1237 6

Peroxisome proliferator-activated receptor gamma (PPARgamma), a member of the superfamily of nuclear receptor transcription factors, plays a critical role in the regulation of the expression of genes associated with inflammation. Using mucous acinar cells of sublingual salivary gland, we investigated the effect of PPARgamma activation on the disturbances in salivary mucin synthesis evoked by lipopolysaccharide (LPS) of periodontopathic bacterium, P. gingivalis. Exposure of the acinar cells to the LPS led to a dose-dependent decrease (up to 58.4%) in mucin synthesis, accompanied by a massive enhancement in apoptosis and NO production, and an induction in inducible nitric oxide synthase (NOS-2) activity. Activation of PPARgamma with a specific synthetic agonist, ciglitazone, prevented in a dose-dependent fashion the LPS-induced reduction in mucin synthesis, and the effect was reflected in a marked decrease in apoptosis, NO generation, and the expression of NOS-2 activity. The impedance by ciglitazone of the LPS-induced changes in mucin synthesis was blocked by PD98059, an inhibitor of extracellular signal regulated kinase (ERK), as well as wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K). Moreover, both agents caused further enhancement in the LPS-induced nitric oxide generation and countered the inhibitory effect of ciglitazone on the LPS-induced upregulation in NOS-2. The findings suggest that the impedance of P. gingivalis LPS inhibition of salivary, mucin synthesis by PPARgamma agonist, ciglitazone, involves activation of ERK pathway by PI3K.
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PMID:Activation of peroxisome proliferator-activated receptor gamma impedes Porphyromonas gingivalis lipopolysaccharide interference with salivary mucin synthesis through phosphatidylinositol 3-kinase/erk pathway. 1267 15

Peroxisome proliferator-activated receptor gamma (PPARgamma) plays a critical role in the regulation of the expression of genes associated with inflammation. In this study, we report that PPARgamma activation leading to the impedance of H. pylori lipopolysaccharide (LPS) inhibitory effect on gastric mucin synthesis occurs with the involvement of phosphatidylinositol 3-kinase (PI3K) and extracellular signal-regulated kinase (ERK) pathways. Using gastric mucosal cells in culture, we show that activation of PPARgamma with a specific synthetic agonist, ciglitazone, prevents in a dose-dependent fashion (up to 90.2%) the LPS-induced reduction in mucin synthesis, and the effect is reflected in a marked decrease in the LPS-induced apoptosis (72.4%), NO generation (80.1%), and the expression of NOS-2 activity (90%). The impedance by ciglitazone of the LPS-induced reduction in mucin synthesis was blocked by wortmannin, a specific inhibitor of P13K and PD98059, an inhibitor of ERK. Both inhibitors, moreover, caused further enhancement in the LPS-induced NO generation and countered the inhibitory effect of ciglitazone on the LPS-induced upregulation in NOS-2. Our findings point to PI3K and ERK as mediators of PPARgamma agonist effect leading to the impedance of H. pylori LPS inhibition on gastric mucin synthesis.
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PMID:Impedance of Helicobacter pylori lipopolysaccharide interference with gastric mucin synthesis by peroxisome proliferator-activated receptor gamma activation involves phosphatidylinositol 3-kinase/ERK pathway. 1274 91

Leptin, a multifunctional hormone produced predominantly by adipocytes but also identified throughout the glandular tissue of alimentary tract, including salivary glands and oral mucosa, has emerged recently as an important regulator of mucosal inflammatory responses to bacterial infection. In this study, we report that leptin prevents (up to 88.4%) the reduction in mucin synthesis evoked in mucous cells of sublingual salivary gland by LPS of periodontopathic bacterium, Porphyromonas gingivalis. The effect of leptin, moreover, was reflected in a marked decrease in the LPS-induced apoptosis, expression of TNF-alpha, caspase-3 activity, and NO generation. The impedance by leptin of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an inhibitor of PI3K, which also obviated the inhibitory effect of leptin on the LPS-induced upregulation in apoptosis, caspase-3 activity, and NO generation. A potentiation in the impedance by leptin of the LPS-induced apoptosis, caspase-3 activity, and NO generation was, however, attained with NOS-2 inhibitor, 1400W, that also caused further enhancement in the impedance by leptin of the LPS detrimental effect on mucin synthesis. Taken together, our data are the first to demonstrate the nature of the involvement of leptin in countering the pathological consequences of P. gingivalis infection on the synthesis of salivary mucins.
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PMID:Leptin suppresses Porphyromonas gingivalis lipopolysaccharide interference with salivary mucin synthesis. 1465 85

Platelet-activating factor (PAF) is now recognized as the most proximal mediator of cellular events triggered by bacterial infection. In this study, we report that a specific PAF antagonist, BN52020, impedes the reduction in mucin synthesis evoked in gastric mucosal cells by H. pylori LPS. The impedance by BN52020 of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an inhibitor of phosphatidylinositol 3-kinase (P13K), which also obviated the inhibitory effect of BN52020 on the LPS-induced upregulation in apoptosis, TNF-alpha, and NO generation. A reduction in the impedance by BN52020 of the LPS detrimental effect on mucin synthesis was also attained with cNOS inhibitor, L-NNA, whereas NOS-2 inhibitor, 1400W caused a potentiation in the impedance effect of BN52020. However, while 1400W and BN52020 countered the potentiating effect of wortmannin on the LPS-induced decrease in mucin synthesis, a further exacerbation of the potentiating effect of wortmannin was attained in the presence of cNOS inhibitor, L-NNA. Our findings suggest that PAF, through the interference with PI3K-dependent cNOS activation, plays a critical role in influencing the extent of pathological consequences of H. pylori infection on the synthesis of gastric mucin.
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PMID:Platelet-activating factor mediates Helicobacter pylori lipopolysaccharide interference with gastric mucin synthesis. 1499 79

Peroxisome proliferator-activated receptor-gamma (PPARgamma), a member of the subfamily of ligand-dependent nuclear transcription factors, plays a key role in the regulation of the expression of genes associated with inflammation. In this study, using gastric mucosal cells in culture, we assess the role of PPARgamma in the disturbances in gastric mucin synthesis and apoptotic processes evoked by Helicobacter pylori lipopolysaccharide (LPS). Exposure of gastric mucosal cells to the LPS led to a concentration-dependent decrease (up to 59.5%) in mucin synthesis, and this effect of the LPS was accompanied by a 6.5-fold increase in apoptosis, induction of COX-2 and NOS-2 protein expression, and the enhancement in PGE(2) generation (18.6-fold) and NOS-2 activity (24.1-fold). However, the expression of COX-1 protein was not affected. Activation of PPARgamma with a specific synthetic agonist, ciglitazone, countered (up to 90.2%) the LPS-induced reduction in mucin synthesis in a concentration-dependent manner, and this effect of the agent was reflected in a marked decrease in COX-2 and NOS-2 protein expression, reduction (up to 72.4%) in apoptosis and a decline (up to 84.1%) in PGE(2) generation and NOS-2 activity (up to 90%). A pronounced prevention (88.2%) in the LPS-induced PGE(2) release and the diminished COX-2 protein expression was also attained with the COX-2-selective inhibitor NS-398, but the effect was not associated with the impedance of the LPS inhibitory effect on mucin synthesis. Our findings thus demonstrate that the detrimental influence of H. pylori LPS on gastric mucin synthesis is closely linked to the increase in proapoptotic processes triggered by NOS-2 upregulation, and that PPARgamma activation obviates this detrimental effect. Hence, pharmacological manipulation of PPARgamma activation may provide therapeutic benefits in countering the disruptive effects of H. pylori on gastric mucosal mucus coat continuity.
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PMID:Peroxisome proliferator-activated receptor gamma activation counters the detrimental effect of Helicobacter pylori lipopolysaccharide on gastric mucin synthesis. 1503 5

Platelet -activating factor (PAF), a phospholipid-derived messenger molecule, is now recognized as the most proximal mediator of cellular events triggered by bacterial lipopolysaccharide (LPS) stimulation. In this study, we assessed the role of PAF in the disturbances in salivary mucin synthesis evoked by LPS of periodontopathic bacterium, P. gingivalis. Using primary culture of mucous acinar cells of sublingual salivary gland, we show that a specific PAF antagonist, BN52020, prevents in a dose-dependent fashion (up to 83.7%) the LPS-induced reduction in mucin synthesis, and the effect is reflected in a marked decrease in the LPS-induced apoptosis (74.8%), NO generation (82.6%), and the expression of TNF-alpha (76.1%). The impedance by BN52020 of the LPS inhibitory effect on mucin synthesis was blocked by wortmannin, an inhibitor of phosphatidylinositol 3-kinase (PI3K), which also obviated the inhibitory effect of BN52020 on the LPS-induced upregulation in apoptosis, TNF-alpha, and NO. A potentiation in the impedance by BN52020 of the LPS detrimental effect on mucin synthesis was however attained with NOS-2 inhibitor, 1400W, while cNOS inhibitor, L-NNA caused a reduction in the impedance effect of BN52020. However, while 1400W and BN52020 countered the potentiating effect of wortmannin on the LPS-induced decrease in mucin synthesis, a further exacerbation of the effect of wortmannin occurred in the presence of L-NNA. The findings implicate PAF as a pivotal factor affecting the extent of pathological consequences of P. gingivalis infection on salivary glands capacity for mucin production, and suggest that its release in response to the LPS serves as a negative regulator of PI3K controlling the pathway of cNOS activation.
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PMID:Platelet-activating factor mediates Porphyromonas gingivalis lipopolysaccharide interference with salivary mucin synthesis via phosphatidylinositol 3-kinase-dependent constitutive nitric-oxide synthase activation. 1508 69

The role of nitric oxide (NO) in inflammatory bowel diseases has traditionally focused on the inducible form of NO synthase (iNOS). However, the constitutive endothelial (eNOS) and neuronal (nNOS) isoforms may also impact on colitis, either by contributing to the inflammation or by regulating mucosal integrity in response to noxious stimuli. To date, studies examining the roles of the NOS isoforms in experimental colitis have been conflicting, and the mechanisms by which these enzymes exert their effects remain unclear. To investigate and clarify the roles of the NOS isoforms in gut inflammation, we induced trinitrobenzenesulfonic acid colitis in eNOS, nNOS, and iNOS knockout (KO) mice, assessing the course of colitis at early and late times. Both eNOS and iNOS KO mice developed a more severe colitis compared with wild-type mice. During colitis, iNOS expression dramatically increased on epithelial and lamina propria mononuclear cells, whereas eNOS expression remained localized to endothelial cells. Electron and fluorescence microscopy identified bacteria in the ulcerated colonic mucosa of eNOS KO mice, but not in wild-type, iNOS, or nNOS KO mice. Furthermore, eNOS KO mice had fewer colonic goblet cells, impaired mucin production, and exhibited increased susceptibility to an inflammatory stimulus that was subthreshold to other mice. This susceptibility was reversible, because the NO donor isosorbide dinitrate normalized goblet cell numbers and ameliorated subsequent colitis in eNOS KO mice. These results identify a protective role for both iNOS and eNOS during colitis, with eNOS deficiency resulting in impaired intestinal defense against lumenal bacteria and increased susceptibility to colitis.
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PMID:Relative contributions of NOS isoforms during experimental colitis: endothelial-derived NOS maintains mucosal integrity. 1521 83


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