Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UNIPROT:P15088 (mast cell)
 14,925 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The objectives of this study were to determine 1) whether the leukocyte-endothelial cell adhesion in postcapillary venules elicited by copper-oxidized low-density lipoproteins (Cu-LDL) is accompanied by enhanced vascular albumin leakage and mast cell degranulation and 2) whether nitric oxide (NO) donors attenuate the Cu-LDL-induced microvascular dysfunction. Infusion of Cu-LDL, but not normal LDL, caused significant increases in leukocyte rolling, adherence, emigration, mast cell degranulation, and an enhanced albumin leakage in rat mesenteric venules. Treatment with the NO donors sodium nitroprusside and spermine-NO or pretreatment with superoxide dismutase or L-arginine significantly reduced the Cu-LDL-induced leukocyte adherence, emigration, mast cell degranulation, and albumin leakage, whereas spermine and D-arginine had no effect. These results indicate that NO protects the microvasculature against the deleterious effects of oxidized LDL, an effect that may be related to NO's ability to reduce leukocyte-endothelial cell adhesion and/or prevent mast cell degranulation.
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PMID:Modulation of oxidized low-density lipoprotein-induced microvascular dysfunction by nitric oxide. 773 66

Lymphoreticular neoplasms of the larynx are rare and comprise a heterogeneous group of tumors. A systematic survey of the literature and autoptic evaluation of the larynx in a relatively small number of patients with systemic lymphoreticular malignancies yielded the following findings: Primary tumors of the larynx must be clearly distinguished from laryngeal involvement by systemic or leukemic infiltrations. By far the most common primary hemopoietic tumors of the larynx are extramedullary plasmacytoma (about 90 cases published) and non-Hodgkin's lymphoma (NHL; about 65 cases published). Primary Hodgkin's disease, granulocytic sarcoma and mast cell sarcoma are extremely rare at this site. Plasmacytoma and NHL both preferentially involve the supraglottis. The subglottis is infrequently affected. Laryngeal plasmacytoma and NHL usually present clinically as localized stage IE and IIE tumors that exhibit no significant tendency to recur or generalize. The therapy of choice is local irradiation while chemotherapy should be reserved for recurrent or progressive disease. Prognosis is favourable in most cases of primary laryngeal plasmacytoma and NHL. Secondary involvement of the larynx by systemic lesions or leukemic infiltrations is usually associated with a very poor prognosis. The prognosis of patients with laryngeal involvement in acute or chronic myeloid leukemia is always poor. Although the histopathological diagnoses given in many case reports are often difficult to compare because of differences in terminology, there seems to be a marked preponderance of B-cell tumors of high-grade malignancy (centroblastic or immunoblastic lymphoma in the Kiel classification of NHL) that probably represents lymphomas originating from mucosa-associated lymphoid tissue (MALT).(ABSTRACT TRUNCATED AT 250 WORDS)
HNO 1994 Jul
PMID:[The larynx in lymphoproliferative and myeloproliferative diseases. Part II: Laryngeal autopsy findings and discussion]. 792 29

We have investigated the contractile effect of bradykinin (BK) in guinea pig lung in vitro. BK induces a dose-related contraction of lung parenchymal strips which is increased significantly in the presence of 10(-5) M captopril (an angiotensin converting enzyme inhibitor) or 10(-5) M DL-thiorphan (a neutral endopeptidase inhibitor). The kininase I inhibitor, DL-2-mercaptomethyl-3-guanidino-ethylthiopropionic acid (MGTPA), has no effect on the BK-induced contraction. BK is more potent in contracting parenchymal lung strips than other contractile agents (histamine, carbachol and substance P), however the BK-induced maximal contraction is lower than those obtained with histamine and carbachol. The B1 agonist, des-Arg9-BK, does not contract lung parenchymal strips. The new BK B2 receptor antagonists (Hoe 140, NPC 17731 and NPC 17761), which possess binding affinities in the nanomolar range, inhibit the BK-induced contractile response in a dose-dependent manner. The BK-induced contraction was unaffected by propranolol, atropine, tetrodotoxin, capsaicin pre-treatment, triprolidine, methysergide, Ro 19-3704 and N omega-nitro-L-arginine-methyl-ester (L-NAME), excluding the involvement of nervous pathways, preformed mast cell mediators, platelet-activating factor and nitric oxide. However, indomethacin, a cyclooxygenase inhibitor, AA-861, a 5-lipoxygenase inhibitor, and furegrelate, a thromboxane A2 synthase inhibitor, decreased the contractile response to BK, suggesting that both cyclooxygenase and 5-lipoxygenase products are involved in this contraction.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Bradykinin-induced contraction of guinea pig lung in vitro. 799 Sep 78

Lymphoreticular neoplasms of the larynx are rare and comprise a heterogeneous group of tumors. A systematic survey of the literature and autoptic evaluation of the larynx in a relatively small number of patients with systemic lymphoreticular malignancies yielded the following findings: Primary tumors of the larynx must be clearly distinguished from laryngeal involvement by systemic or leukemic infiltrations. By far the most common primary hemopoietic tumors of the larynx are extramedullary plasmacytoma (about 90 cases published) and non-Hodgkin's lymphoma (NHL; about 65 cases published). Primary Hodgkin's disease, granulocytic sarcoma and mast cell sarcoma are extremely rare at this site. Plasmacytoma and NHL both preferentially involve the supraglottis. The subglottis is infrequently affected. Laryngeal plasmacytoma and NHL usually present clinically as localized stage IE and IIE tumors that exhibit no significant tendency to recur or generalize. The therapy of choice is local irradiation while chemotherapy should be reserved for recurrent or progressive disease. Prognosis is favorable in most cases of primary laryngeal plasmacytoma and NHL. Secondary involvement of the larynx by systemic lesions or leukemic infiltrations is usually associated with a very poor prognosis. The prognosis of patients with laryngeal involvement in acute or chronic myeloid leukemia is always poor. Although the histopathological diagnoses given in many case reports are often difficult to compare because of differences in terminology, there seems to be a marked preponderance of B-cell tumors of high-grade malignancy (centroblastic or immunoblastic lymphoma in the Kiel classification of NHL) that probably represents lymphomas originating from mucosa-associated lymphoid tissue (MALT).(ABSTRACT TRUNCATED AT 250 WORDS)
HNO 1994 Jun
PMID:[The larynx in lymphoproliferative and myeloproliferative diseases. I: An overview with special reference to primary laryngeal malignant lymphomas and plasmacytomas]. 807 Oct 93

Treatment 20 min beforehand with an inhibitor of nitric oxide (NO) synthesis NW-nitro-1-arginine methyl ester (L-NAME) (12.5, 25, 50 or 100 mg/kg, s.c.), dose-dependently intensified gastric glandular mucosal ulceration produced by cold-restraint stress. Hexamethonium (20 mg/kg) or atropine (1 mg/kg) pretreatment s.c. 20 min before stress strongly antagonised stress-evoked ulceration, as well as the ulcer-potentiating effects of L-NAME when either cholinoceptor antagonist was given concurrently with the NO inhibitor. Stress-induced mast cell degranulation was not worsened by L-NAME pretreatment. The findings suggest that NO could confer partial protection against stress-induced gastric ulcer formation; its activity is triggered off by the ulcerogenic mechanism of stress.
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PMID:Nitric oxide inhibition intensifies cold-restraint induced gastric ulcers in rats. 809 77

Leukocyte-endothelial cell adhesion and an altered metabolism of endothelial cell-derived nitric oxide (NO) have been implicated in the microvascular dysfunction associated with ischemia/reperfusion (I/R). The objective of this study was to determine whether NO donors can attenuate the reperfusion-induced increase in venular albumin leakage via an effect on leukocyte-endothelial cell adhesion. Leukocyte adherence and emigration as well as albumin extravasation were monitored in single postcapillary venules in rat mesentery subjected to 20 minutes of ischemia followed by 30 minutes of reperfusion. This I/R protocol elicits significant leukocyte adherence and emigration as well as a profound albumin leakage response. Superfusion of the mesenteric microcirculation with the NO donors sodium nitroprusside, spermine-NO, and SIN1 significantly reduced the I/R-induced leukocyte adherence/emigration and albumin leakage in postcapillary venules, whereas neither spermine nor the NO synthase inhibitor NG-nitro-L-arginine methyl ester affected the I/R-induced responses. Platelet-leukocyte aggregation and mast cell degranulation were also observed in the postischemic mesentery, and the responses were also attenuated by the NO donors. Plasma nitrate/nitrite levels in the superior mesenteric vein were significantly reduced by I/R. The results of this study indicate that I/R-induced microvascular dysfunction (albumin leakage) is attenuated by NO and that the protective effect of NO donors may be related to their ability to reduce leukocyte-endothelial cell and leukocyte-platelet interactions and/or mast cell degranulation.
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PMID:Modulation of ischemia/reperfusion-induced microvascular dysfunction by nitric oxide. 811 46

In this study, we assessed the involvement of mast cells and mast cell-derived mediators in the enhanced epithelial permeability associated with nitric oxide synthesis inhibition. Permeability of the small bowel was assessed by measuring the clearance of a small marker (51Cr-labeled EDTA) from blood to lumen in the presence of the nitric oxide synthesis inhibitor, NG-nitro-L-arginine methyl ester (L-NAME). L-NAME caused a very rapid (10 min) increase in epithelial permeability, reaching peak values (sixfold increase) within 20 min. Two mast cell stabilizers, doxantrazole and lodoxamide, greatly attenuated the rise in mucosal permeability. Rat mast cell protease II activity (marker of mucosal mast cell degranulation) was increased significantly only in the plasma of L-NAME-treated animals. Chronic dexamethasone administration depleted rats of mucosal mast cells and also prevented the L-NAME-induced rise in mucosal permeability. The increase in epithelial permeability was mediated by a number of mediators: platelet-activating factor caused the early rise in epithelial permeability, and histamine caused the later increase in epithelial permeability. Superoxide dismutase attenuated the L-NAME-induced rise in epithelial permeability, suggesting an important and continuous role for superoxide. Transepithelial flux of 51Cr-EDTA across rat intestinal epithelial cell monolayers did not increase in the presence of L-NAME, suggesting that inhibition of nitric oxide does not directly cause epithelial permeability alterations, whereas the in vivo data implicate a potential role for the mast cell. In conclusion, nitric oxide synthesis inhibition activates mast cells in the mucosa and consequently increases epithelial permeability.
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PMID:Nitric oxide synthesis inhibition increases epithelial permeability via mast cells. 814 Dec 95

Release of inflammatory mediators by mast cells can be modulated by certain cytokines and by nitric oxide. An in vitro platelet aggregation bioassay was used to assess the effects of interleukin-1 beta (IL-1 beta) on the release of platelet-activating factor and nitric oxide from resting or ionophore-activated peritoneal mast cells (PMC) from rat. PMC spontaneously released a substance that inhibits thrombin-stimulated platelet aggregation. The activity of this substance is abolished by addition of hemoglobin to the platelet suspension and augmented by preincubation of the PMC with L-arginine, suggesting that it is nitric oxide. Within minutes, IL-1 beta concentration-dependently (1 pg/ml-100 ng/ml) enhanced the release from activated PMC of nitric oxide, as measured by its ability to inhibit thrombin-induced platelet aggregation, and as confirmed with a biochemical assay for nitrite. This action of IL-1 beta was inhibited by pretreatment of PMC with a calmodulin antagonist (calmidazolium), an IL-1 receptor antagonist, or either of two nitric oxide synthase inhibitors (L-NAME and LY-83583). IL-1 beta also inhibited the release of platelet-activating factor from PMC through a nitric-oxide-dependent mechanism. These results demonstrate that IL-1 beta is a potent and rapid-acting modulator of mast cell reactivity, stimulating nitric oxide release while inhibiting the production of platelet-activating factor.
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PMID:Modulation of rat mast cell reactivity by IL-1 beta. Divergent effects on nitric oxide and platelet-activating factor release. 839 60

Recent work has demonstrated that inhibition of nitric oxide production with various nitric oxide synthesis inhibitors (L-NAME, L-NMMA) initiate leukocyte adhesion to postcapillary venules. The objective of this study was to elucidate the mechanism (or mechanisms) that promote the L-NAME-induced leukocyte response. Intravital microscopy was used to examine 25-40 microns venules in the rat mesentery. Nitric oxide synthesis was inhibited with L-NAME and leukocyte adhesion was observed over the first 60 min. The fourfold increase in leukocyte adhesion was independent of alterations in venular red blood cell velocity. The adhesion was superoxide-mediated inasmuch as superoxide dismutase (SOD) abolished the rise in leukocyte adhesion associated with nitric oxide synthesis inhibition. Ketotifen, a mast cell stabilizer, also abolished the rise in leukocyte adhesion induced by L-NAME. Histology revealed that mast cell degranulation occurred only in animals treated with L-NAME but not in animals pretreated with SOD or ketotifen. This observation suggests that mast cells become activated in the absence of nitric oxide production and superoxide contributes to the mast cell activation. The L-NAME-induced leukocyte adhesion could be reproduced by infusing hypoxanthine/xanthine oxidase (a superoxide generating system) or compound 48/80 (an activator of mast cells) and both responses were attenuated by ketotifen. These data suggest that inhibition of nitric oxide synthesis results in a superoxide and mast cell-dependent leukocyte adhesion.
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PMID:Nitric oxide synthesis inhibition induces leukocyte adhesion via superoxide and mast cells. 840 15

The effects of mast cell granules (MCGs) on macrophage-mediated lysis of P815 mastocytoma cells and nitric oxide (NO) production were studied. Murine peritoneal macrophages exhibited tumor cell killing and NO production only when activated with lipopolysaccharide (LPS) or interferon-gamma (IFN-gamma). Coincubation of macrophages with MCGs during LPS activation dose-dependently inhibited macrophage-mediated tumor cell lysis. The MCG effect was not due to inactivation or removal of LPS by MCG. The inhibitory effect was also not due to histamine or serotonin present in the MCGs. The granules were not toxic to macrophages or P815 mastocytoma cells. The effect of MCGs on macrophage-mediated tumor cell killing was evident whether MCGs were added before or after a 4-h exposure of macrophages to LPS. However, the inhibitory effect was not seen if MCGs were added after macrophages had been exposed to LPS for 24 h. To assess whether MCGs could inhibit a non-LPS trigger, MCGs were tested on macrophages activated with IFN-gamma. In these experiments, MCGs dose-dependently inhibited macrophage-mediated tumor cell killing induced by IFN-gamma, LPS, or IFN-gamma plus LPS. Furthermore, in parallel experiments, MCGs significantly inhibited macrophage NO production induced by LPS, IFN-gamma, or IFN-gamma plus LPS. Pretreatment of MCGs with diisopropylfluorophosphate, a serine protease inhibitor, only partially abrogated the effects of MCGs. The results demonstrate that MCGs inhibit both LPS- and IFN-gamma-induced macrophage killing of P815 cells and the inhibition is associated with the decrease of NO production.
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PMID:Mast cell granules inhibit macrophage-mediated lysis of mastocytoma cells (P815) and nitric oxide production. 848 25


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