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)

Using fibroblastic CHO cells, we have examined 1) the internalization and redistribution of surface binding sites for the lectins Concanavalin A and wheat germ agglutinin and 2) the sensitivity of these processes to putative inhibitors of cytoskeletal activity. Following initial exposure to fluorescein conjugated Con A (CAF) or WGA (WGAF) at 4 degrees C, kinetic analysis of internalization and intracellular aggregation of lectin at 37 degrees C indicated more rapid aggregate formation in the case of WGA than in the case of Con A. Treatment with tertiary amine local anesthetics (tetracaine, dibucaine, and xylocaine) or with a lysosomatrophic amine, m-dansyl cadaverine, blocked internalization of Con A but not of WGA. Similar differential effects on redistribution of Con A and WGA were not however observed with the antimicrotubule agents colchicine and nocodazole. Simultaneous treatment of cells with WGAF and with rhodamine labeled Con A (CAR) resulted in the accumulation of both labels in a central perinuclear aggregate; a similar experiment in the presence of local anesthetic resulted in a diffuse peripheral distribution of CAR and a central aggregate of WGAF. These results suggest 1) CHO cells possess at least two distinct pathways for lectin internalization and redistribution, which can be discriminated in terms of drug sensitivity; 2) CHO cells can sort out and independently internalize different populations of lectin binding sites; and 3) different pathways may be a manifestation of biochemically distinct linkages between cytoskeletal elements and various groups of surface glycoproteins. Present findings concur with our previous results concerning the mutual independence of the surface binding sites for Con A and WGA (Emerson and Juliano, 1982).
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PMID:Interactions of lectins with CHO cell surface membranes. II. Differential effects of local anesthetics on endocytosis of Con A and WGA binding sites. 704 42

We aimed to show whether the administration of exogenous L-Arg would alter the morphological, functional changes and interaction of nitric oxide and cell adhesion molecules such as tenascin and lectin after release of twenty-four hours complete ureteric obstruction in the solitary rat kidney tissue. Forty prepubertal Wistar-Albino rats were separated into 4 groups, each containing 10 rats. In the group 1 (Sham-control, n = 10), right nefrectomy was performed; the left ureter was visualized but not ligated. In the remaining 30 rats, the abdomen was opened and undergone right nephrectomy and the left ureter was completely obstructed. After 24 hours, thirty rats were divided as group 2, 3, and 4, each containing 10 rats. In-group 2, no drug treatments were given. In-group 3 L-Arg (L-arginine methyl ester) was infused immediately after abolishing ureteric obstruction. In-group 4 L-NAME was give separately during L-Arg administration during 30 minutes immediately after abolishing ureteric obstruction. Than, the animals were prepared for functional and histopathological studies. BUN value was decreased significantly in L-Arg group when compared with untreatment and L-NAME groups (p < 0.05, p < 0.001 respectively). Creatinine values were decreased in L-Arg group when compared with untreatment group (p < 0.002). Urine flow and urinary Na value was increased significantly in L-Arg group when compared to other obstruction groups (p < 0.001, p < 0.001). The increase in the number of macrophages in Untreated and L-NAME group were significant (p < 0.001, p < 0.001) when compared to L-Arg group. Immunohistochemical study showed that tenascin and lectin expression was severe in tubulus basal membrane of untreated and L-NAME treated rats. In L-Arg group, tenascin and lectin expression was moderate in tubulus membrane. Our results suggest that the administration of exogenous L-Arg protect the functional and degenerative effects of acute complete obstruction in the solitary kidney tissue of the rats. Nitric oxide cause these positive effects by decreasing preglomerular vascular resistance, regulation of neutrophil function and preventing the expression of cell adhesion molecules such as tenascin and lectin.
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PMID:Interaction of nitric oxide and cell adhesion molecules after 24 hours of complete ureteric obstruction in the rats on a solitary kidney. 1223 Feb 67

Intimal infiltration by monocytes and accumulation of lipids represent a critical step in the formation of fatty streaks during atherogenesis. Because elevated plasma levels of asymmetric dimethylarginine (ADMA), a potent nitric oxide (NO) synthase (NOS) inhibitor, are prevalent in diverse cardiovascular diseases, the goal of this study was to examine the contribution of NO deficiency to macrophage lipid accumulation. Inhibition of NO synthesis in PMA-primed human monocytic leukemia HL-60 cells resulted in a twofold increase in expression of the receptor for oxidized LDL (OxLDL), termed the lectin-like OxLDL receptor (LOX-1). Blockade of inducible NOS in activated macrophages resulted in 1,1'-dioctadecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI)-OxLDL accumulation and imparted macrophages with a foamy appearance as detected with oil-red O lipid staining. ADMA (15 microM) or N(G)-nitro-l-arginine methyl ester (l-NAME, 300 microM), both of which suppress inducible NOS activity, increased oil-red staining 1.9- and 2.8-fold, respectively. Macrophages treated with ADMA or l-NAME showed a 2.4-fold increase in accumulation of DiI-OxLDL. To examine the role of LOX-1 in this process, we used small interfering RNA (siRNA) duplex-mediated LOX-1 gene silencing. LOX-1 expression was suppressed twofold by siRNA as shown by Western blot analysis. This suppression was associated with a two- to fourfold decrease in DiI-OxLDL uptake as identified by fluorescence microscopy and decreased oil-red O staining by activated macrophages. In conclusion, accumulation of ADMA (a competitive inhibitor of NOS) in patients with chronic renal failure may be responsible for upregulation of LOX-1 receptor and increased OxLDL uptake, thus contributing to lipidosis and foam cell formation. The data illustrate an additional nonendothelial mode of antiatherogenic action of NO: prevention of LOX-1 induction and lipid accumulation by macrophages.
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PMID:Asymmetric dimethylarginine upregulates LOX-1 in activated macrophages: role in foam cell formation. 1501 31

We have investigated the vascular relaxant effects of the lectin from a red marine alga Bryothamnion triquetrum (BTL), in particular, the endothelial-dependency and the participation of a specific glycoprotein-binding site. BTL (1-100 microg mL(-1)) was applied to rat isolated aortic rings, with or without endothelium, tonically precontracted with phenylephrine (0.1 microM). Endothelium-dependent relaxation was assessed in the presence of indometacin (10 microM), L-nitro arginine methyl ester (L-NAME, 100 microM) and tetraethylammonium (TEA, 500 microM). For the involvement of the glycoprotein-binding site, BTL was assayed in presence of mucin (300 microg mL(-1)) or N-acetyl D-glucosamine (GlcNAc; 300 microg mL(-1)), a specific and non-specific lectin-binding sugar, respectively. BTL fully and concentration dependently relaxed preparations that possessed an intact endothelium (IC50 (concn producing 50% contraction) = 12.1 +/- 1.6 microg mL(-1)), whereas no significant relaxation was observed in endothelial-denuded tissue. L-NAME, but not indometacin or TEA, completely inhibited the lectin relaxation, suggesting the involvement of nitric oxide (NO). The lectin in association with mucin, but not with GlcNAc, inhibited BTL-induced relaxation, implicating the involvement of the lectin binding site. Our data suggest that the relaxant effect of the red marine alga Bryothamnion triquetrumlectin on isolated aorta occurs via interaction with a specific lectin-binding site on the endothelium, resulting in a release of NO.
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PMID:Red marine alga Bryothamnion triquetrum lectin induces endothelium-dependent relaxation of the rat aorta via release of nitric oxide. 1552 48

The aim of this study is to evaluate histopathological findings induced by Nomega-nitro-L-arginine methyl ester (L-NAME) and molsidomine (MOL) on the kidney of bile duct ligated rats. Forty Sprague-Dawley rats, each weighing 125 to 140 g, were included in the study. Extent of histological glomerular injury scores (GIS), arterial injury scores (AIS), and tubulointerstitial injury scores (TIS) in each animal were graded. Alpha-smooth muscle actin (alpha-SMA), tenascin, lectin (Ulex europaeus agglutinin-1), and vimentin were used to determine extent of the injury. The cholestasis was evidenced by a significant increase in the levels of serum total bilirubin in BDL rats (p < 0.01). Malondialdeyde MDA levels increased by the bile duct ligation (BDL) to 12.10 +/- 0.45. This value was significantly higher than the other groups (p < 0.01). Changes in the BDL kidney were marked at 7 days after surgery. GIS were observed to have the highest score, especially at juxtamedullary region in BDL/L-NAME rats, and AIS were also the highest score in this region. These observations were lower in BDL/MOL rats. There is a correlation between GIS and AIS scores (r = .2, p < .01). TIS revealed that BDL/L-NAME rats were significantly more damage than rats in the other groups (p<.001). MOL-treated rats showed considerably fewer lesions in the tubules and interstitium (p < .001). The tubular injuries observed in BDL and BDL/L-NAME rats were significantly attenuated by MOL treatment. Lectin was more and extensively stained in tubular epithelia of the BDL/L-NAME group than in the other (p <.05). Expression of tenascin in tubular epithelia was significantly higher in BDL and BDL/L-NAME as compared with controls (p < .01). Fibrous tissue was only observed in the BDL and BDL/L-NAME group. These areas were weakly stained with vimentin. alpha-SMA staining was more reduced in the L-NAME-treated arterioles than in BDL/MOL (p < .05). In conclusion, the analysis of cell injury based on a histological grading system in the model of BDL kidney allows the quantification of the degree of injury.
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PMID:Does the analysis based on a histological and immunohistochemical grading system in the model of BDL kidney allow the quantification of the degree of injury? 1552 6

PPAR-gamma agonists (thiazolidinediones, TZDs) may improve endothelial function independently of insulin sensitizing. Bone marrow-derived endothelial progenitor cells (EPC) contribute to neoangiogenesis. Mice were treated with pioglitazone, 20mg/kg/day for 10 days. Treatment with TZD upregulated circulating Sca-1/VEGFR-2 positive EPC in the blood (235+/-60%) and the bone marrow (166+/-30%), cultured spleen-derived DiLDL/lectin positive EPC increased to 231+/-21% (n=24 per group). Upregulation of EPC was persistent after 20 days. TZD increased SDF-1-induced migratory capacity per number of EPC by 246+/-73% and increased expression of telomere repeat-binding factor 2 by 320+/-50%. In vivo neoangiogenesis was increased two-fold (214+/-42%, 20 days). The NOS inhibitor L-NAME did not inhibit the TZD-induced upregulation of EPC. EPC from TZD-treated animals showed reduced in vivo apoptosis (65+/-2.8% of vehicle). In cultured human EPC, pre-treatment with pioglitazone prevented H(2)O(2)-induced apoptosis. Inhibition of EPC apoptosis by TZD was abolished in the presence of wortmannin but not by LNMA. In summary, TZD upregulates both number and functional capacity of endothelial progenitor cells. Pioglitazone prevents apoptosis of EPC in mice as well as in human EPC in a PI3K-dependent but NO-independent manner. Reduction of EPC apoptosis by TZD may be a potentially beneficial mechanism for patients with vascular diseases.
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PMID:The PPAR-gamma agonist pioglitazone increases neoangiogenesis and prevents apoptosis of endothelial progenitor cells. 1687 72

A novel 14-kDa lectin from Annona coriacea seeds (ACLEC) with hemagglutinating activity on erythrocytes has been recently described. Since plant lectins are known to present inflammatory activity, this study aimed to investigate the leukocyte migration induced by ACLEC, and inflammatory mediators involved in this phenomenon. Male Swiss mice were intraperitoneally injected with ACLEC (3-100 microg/cavity), and at 4-96 h thereafter the leukocyte counts in peritoneal lavage fluid were evaluated. ACLEC induced a dose-dependent neutrophil accumulation, reaching maximal responses at 16 h after injection (approximately 40-fold increase for 30 microg/cavity). Significant accumulation of mononuclear cells was observed at 72 h (2.7-fold increase). The carbohydrate mannose nearly abolished the neutrophil influx, whereas sucrose, glucose and galactose had no effect. Dexamethasone, the cyclooxygenase-2 (COX-2) inhibitor celecoxib and the Platelet activating factor (PAF) receptor antagonist PCA4248 significantly reduced ACLEC-induced neutrophil influx. The tachykinin NK(1) antagonist SR140333, the tachykinin NK(2) antagonist SR48968, the non-selective NO inhibitor L-NAME, the selective inducible NOS inhibitor aminoguanidine and the lypoxygenase inhibitor AA861 all failed to modify the ACLEC-induced responses. In conclusion, ACLEC is able to attract neutrophils into the mice peritoneal cavity by mechanisms involving interactions of the lectin with cell-specific mannose recognition, leading to the release of COX-2-derived mediators and PAF.
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PMID:Neutrophil migration in mice induced by a mannose-binding lectin isolated from Annona coriacea seeds. 1692 40

Bone marrow derived endothelial progenitor cells (EPC) improve endothelial function and neoangiogenesis. Prostaglandin E1 (PGE1) is used for the treatment of patients with peripheral artery disease (PAD). However, the molecular effects are only partially understood. Treatment of C57/Bl6 mice with PGE1, 10 microg/kg BW increased the number of circulating Sca-1/VEGFR-2 positive EPC in the blood compared to vehicle (122+/-7% and 119+/-6% after 10 and 20 days). EPC in the bone marrow were upregulated to 125+/-11% (10 days) and 142+/-15% (20 days). PGE1 increased DiLDL/Lectin positive spleen-derived EPC to 170+/-20% and 174+/-14% after 10 and 20 days. Treatment with PGE1 enhanced in-vivo neoangiogenesis by 2-fold (disk assay, 218+/-27%). PGE1 enhanced the SDF-1 induced migratory capacity per number of EPC to 140+/-11%, 146+/-22% and 160+/-16% after 10, 14 and 20 days. Greater migratory capacity was associated with upregulation of expression of telomere repeat-binding factor (TRF2). EPC of PGE1-treated mice were characterized by reduced apoptosis. Similarly, PGE1 prevented H(2)O(2)-induced apoptosis in cultured human EPC. The effect is mediated by PI3-kinase. The effects of PGE1 on EPC were completely prevented by co-treatment with the NO-inhibitor L-NAME, 50 mg kg(-1) p.o. Treatment with the prostaglandin I2 derivative iloprost (10 microg/kg BW, 20 days) did not alter EPC numbers or function. Physical exercise is the basis of the treatment of patients with PAD. Voluntary running increased EPC numbers in mice. Treatment with PGE1 resulted in an additional increase of Sca-1/VEGFR-2- and DiLDL/lectin positive EPC as well as migration. n=10-24 for all groups, all effects p<0.05. In summary, prostaglandin E1 increases the number of EPC in the blood and the bone marrow in mice. The effect is additive to physical exercise, depends on nitric oxide and is characterized by reduction of PI3-kinase mediated apoptosis. PGE1-mediated upregulation of EPC is associated with improved EPC function and enhanced angiogenesis.
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PMID:Regulation of endothelial progenitor cells by prostaglandin E1 via inhibition of apoptosis. 1729 26

Synthesis of nitric oxide (NO) is one of the important effector functions of innate immune cells. Although several reports have indicated mistletoe lectins induce immune cells to produce cytokines, studies regarding the activities of the lectins in the production of NO have been very limited. Here, we report on the induction of NO synthesis in a murine macrophage cell line, RAW264.7, by Korean mistletoe lectin (KML-IIU). When the macrophage cells were treated with KML-IIU in the presence of a suboptimal concentration of IFN-gamma, NO production was induced in a concentration-dependent manner. Significantly higher levels of NO were induced by subchains of the KML-IIU (A and B), which have lower toxicities, as compared to the hololectin. Furthermore, expression of the inducible nitric oxide synthase (iNOS) gene was elevated in accordance with the level of NO production. When the synthase was inhibited by iNOS inhibitors (L-NIL and L-NAME), NO production was specifically reduced in a concentration-dependent manner. Our studies demonstrate that the KML-IIU and its subchains induce NO production in murine macrophage cells via activation of the iNOS gene expression, suggesting that the KML-IIU subchains may be used as an immunomodulator to enhance the effector functions of innate immune cells.
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PMID:Korean mistletoe lectin (KML-IIU) and its subchains induce nitric oxide (NO) production in murine macrophage cells. 1794 Aug 53

This study investigated and compared vascular actions of leguminous lectins obtained from the Canavalia genus (Canavalia brasiliensis, Canavalia gladiata, and Canavalia maritima) in the rat models of paw edema and isolated aorta. Paw edema was induced by subcutaneous injection of lectins (0.01-1 mg/kg) in animals pre-treated or not with indomethacin or L-NAME. In isolated aorta, cumulative concentration curves of C. gladiata or C. brasiliensis (1-100 microg/ml) were performed at the contraction plateau induced by phenylephrine or at tissue basal tonus. The mechanism of the lectin relaxant action was investigated by previous addition of L-NAME, indomethacin, or tetraethylammonium. In both models, the lectin domain involvement was evaluated by incubation of lectins with their ligand and non-ligand sugars. The lectins induced paw edema paralleled by protein leakage. The edematogenic activity elicited by C. gladiata and C. brasiliensis involves prostaglandins and nitric oxide (NO), while that of C. maritima occurs without NO interference. C. gladiata and C. brasiliensis elicited aorta relaxation involving NO and prostacyclin, while that of C. gladiata included EDHF. All lectin effects were prevented by their binding sugars. The present study demonstrated important vasodilator effects of different degrees and mechanisms in vivo and in vitro of Canavalia lectins. In vivo, the edematogenic activity was paralleled by plasma exudation, and in vitro, aorta relaxation was strictly dependent on intact endothelium. All effects occurred via interaction with lectin domains and participation of NO and/or prostanoids.
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PMID:Vasodilator effects of Diocleinae lectins from the Canavalia genus. 1985 60


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