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Oxidized low density lipoprotein displaces endothelial nitric-oxide synthase (eNOS) from plasmalemmal caveolae and impairs eNOS activation

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第45期274卷 32512-32519页

作者： Blair, A Shaul, PW Yuhanna, IS Conrad, PA Smart, EJ Univ Kentucky Dept Physiol Sch Med Lexington KY 40536 USA Univ Texas SW Med Ctr Dept Pediat Dallas TX 75235 USA Bucknell Univ Dept Biol Lewisburg PA 17837 USA

Hypercholesterolemia-induced vascular disease and atherosclerosis are characterized by a decrease in the bioavailability of endothelium-derived nitric oxide. Endothelial nitric-oxide synthase (eNOS) associates with caveolae and is directly regulated by the caveola protein, caveolin. In the present study, we examined the effects of oxidized low density Lipoprotein (oxLDL) on the subcellular location of eNOS, on eNOS activation, and on caveola cholesterol in endothelial cells. We found that treatment with 10 mu g/ml oxLDL for 60 min caused greater than 90% of eNOS and caveolin to leave caveolae, Treatment with oxLDL also inhibited acetylcholine-indnced activation of eNOS but not prostacyclin production. oxLDL did nob affect total cellular eNOS abundance. Oxidized LDL also did not affect the palmitoylation, myristoylation or phosphorylation of eNOS. Oxidized LDL, but not native LDL, or HDL depleted caveolae of cholesterol by serving as an acceptor for cholesterol. Cyclodextrin also depleted caveolae of cholesterol and caused eNOS and caveolin to translocate from caveolae. Furthermore, removal of oxLDL allowed eNOS and caveolin to return to caveolae. We conclude that oxLDL-induced depletion of caveola cholesterol causes eNOS to leave caveolae and inhibits acetylcholine-induced activation of the enzyme. This process may be an important mechanism in the early pathogenesis of atherosclerosis.

关键词：细胞膜/药物作用细胞膜/酶学细胞培养的胆固醇/代谢环糊精类/药理学内皮血管/药物作用内皮血管/酶学酶激活荧光抗体技术间接脂蛋白类 HDL/代谢脂蛋白类 LDL/代谢肉豆蔻酸/代谢一氧化氮合酶/代谢一氧化氮合酶Ⅲ型棕榈酸/代谢磷酰化猪动物

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Localization of nitric-oxide synthase in plant peroxisomes

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第51期274卷 36729-36733页

作者： Barroso, JB Corpas, FJ Carreras, A Sandalio, LM Valderrama, R Palma, JM Lupiáñez, JA del Río, LA CSIC Estac Expt Zaidin Dept Bioquim Biol Celular & Mol Plantas E-18080 Granada Spain Univ Jaen Fac Ciencias Expt Dept Bioquim & Biol Mol E-23071 Jaen Spain Univ Granada Ctr Ciencias Biol Dept Bioquim & Biol Mol E-18001 Granada Spain

The presence of nitric-oxide synthase (NOS) in peroxisomes from leaves of pea plants (Pisum sativum L.) was studied. Plant organelles were purified by differential and sucrose density gradient centrifugation. In purified intact peroxisomes a Ca2+-dependent NOS activity of 5.61 nmol of L-[H-3]citrulline mg(-1) protein min(-1) was measured while no activity was detected in mitochondria. The peroxisomal NOS activity was clearly inhibited (60-90%) by different well characterized inhibitors of mammalian NO synthases. The immunoblot analysis of peroxisomes with a polyclonal antibody against the C terminus region of murine iNOS revealed an immunoreactive protein of 130 kDa. Electron microscopy immuno-gold-labeling confirmed the subcellular localization of NOS in the matrix of peroxisomes as well as in chloroplasts. The presence of NOS in peroxisomes suggests that these oxidative organelles are a cellular source of nitric oxide (NO) and implies new roles for peroxisomes in the cellular signal transduction mechanisms.

关键词：一氧化氮合酶/分离和提纯一氧化氮合酶/代谢过氧化物酶体类/代谢植物/酶学植物/超微结构

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Rapid inactivation of NOS-I by lipopolysaccharide plus interferon-γ-induced tyrosine phosphorylation

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JOURNAL OF BIOLOGICAL CHEMISTRY 1999年第15期274卷 9915-9917页

作者： Colasanti, M Persichini, T Cavalieri, E Fabrizi, C Mariotto, S Menegazzi, M Lauro, GM Suzuki, H Univ Verona Dipartimento Sci Neurol & Vis Sez Chim Biol Biol Chem Lab I-37134 Verona Italy Univ Rome Dept Biol Roma TRE I-00146 Rome Italy

Human astrocytoma T67 cells constitutively express a neuronal NO synthase (NOS-I) and, following administration of lipopolysaccharide (LPS) plus interferon-gamma (IFN gamma), an inducible NOS isoform (NOS-II). Previous results indicated that a treatment of T67 cells with the combination of LPS plus IFN gamma, by affecting NOS-I activity, also inhibited NO production in a very short time. Here, we report that under basal conditions, a NOS-I protein of about 150 kDa was weakly and partially tyrosine-phosphorylated, as verified by immunoprecipitation and Western blotting. Furthermore, LPS plus IFN gamma increased the tyrosine phosphorylation of NOS-I, with a concomitant inhibition of its enzyme activity. The same effect was observed in the presence of vanadate, an inhibitor of phosphotyrosine-specific phosphatases. On the contrary, genistein, an inhibitor of protein-tyrosine kinases, reduced tyrosine phosphorylation of NOS-I, enhancing its enzyme activity. Finally, using reverse transcriptase-polymerase chain reaction, we have observed that a suboptimal induction of NOS-II mRNA expression in T67 cells was enhanced by vanadate (or L-NAME) and inhibited by genistein. Because exogenous NO has been found to suppress NOS-II expression, the decrease of NO production that we have obtained from the inactivation of NOS-I by LPS/IFN gamma-induced tyrosine phosphorylation provides the best conditions for NOS-II expression in human astrocytoma T67 cells.

关键词：星形细胞瘤/代谢酶诱导染料木黄酮/药理学干扰素γ/药理学脂多糖类/药理学神经组织蛋白质类/代谢一氧化氮合酶/生物合成一氧化氮合酶/代谢一氧化氮合酶Ⅰ型一氧化氮合酶Ⅱ型磷酰化聚合酶链反应 RNA 信使/代谢肿瘤细胞培养的酪氨酸/代谢钒酸盐类/药理学人类

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Interference in MTT cell viability assay in activated macrophage cell line

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ANALYTICAL BIOCHEMISTRY 2003年第2期313卷 338-341页

作者： Pozzolini, M Scarfi, S Benatti, U Giovine, M CNR Direzione Progetto Finalizzato Biotecnol I-16132 Genoa Italy Univ Genoa Dipartimento Med Sperimentale Sezione Biochim I-16132 Genoa Italy

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Regulation of prostaglandin biosynthesis by nitric oxide is revealed by targeted deletion of inducible nitric-oxide synthase

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13427-13430页

作者： Marnett, LJ Wright, TL Crews, BC Tannenbaum, SR Marrow, JD Vanderbilt Univ Sch Med Dept Biochem Nashville TN 37232 USA Vanderbilt Univ Sch Med Dept Med Nashville TN 37232 USA MIT Div Bioengn & Environm Hlth Cambridge MA 02139 USA MIT Dept Chem Cambridge MA 02139 USA

We investigated the effects of targeted deletion of the inducible NO synthase (iNOS) gene on the formation of prostaglandins in vivo and ex vivo. Peritoneal macrophages were obtained from control and iNOS-deficient mice, and prostaglandin E-2 (PGE(2)) was quantified after stimulation with gamma-interferon and lipopolysaccharide to induce COX-a, Total nitrate and nitrite production was completely abolished in cells from iNOS-deficient animals compared with control cells. PGE, formation by cells from MOS-deficient animals was decreased compared with cells from control animals 80% at 12 h (0.85 +/- 0.90 ng/10(6) cells versus 15.4 +/- 2.1 ng/10(6) cells, p < 0.01) and 74% at 24 h (9.4 +/- 4.3 ng/10(6) cells versus 36.8 +/- 4.1 ng/10(6) cells, p < 0.01), COX-2 protein expression was not significantly different in cells from control or knockout animals. Levels of PGE(2) in the urine of iNOS-deficient mice were decreased 78% (0.24 +/- 0.14 ng/mg of creatinine versus 1.09 +/- 0.66 ng/mg of creatinine, p < 0.01) compared with control animals. In addition, the levels of urinary F-2-isoprostanes, an index of endogenous oxidant stress, were significantly decreased in iNOS-deficient animals. In contrast, the levels of thromboxane B-2 derived from platelets allowed to aggregate ex vivo were significantly increased in iNOS-deficient mice compared with wild-type mice. These studies support the hypothesis that NO and/or NO-derived species modulate cyclooxygenase activity and eicosanoid production in vivo.

关键词：细胞培养的环氧化酶2 地诺前列酮/生物合成基因缺失同工酶类/代谢巨噬细胞腹膜/代谢小鼠基因敲除一氧化氮/代谢一氧化氮合酶/遗传学一氧化氮合酶/代谢一氧化氮合酶Ⅱ型前列腺素内过氧化物合酶类/代谢动物小鼠

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Nitric oxide synthase inhibition by N^G-nitro-L-arginine methyl ester inhibits tumor-induced angiogenesis in mammary tumors

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AMERICAN JOURNAL OF PATHOLOGY 1999年第4期155卷 1381-1390页

作者： Jadeski, LC Lala, PK Univ Western Ontario Dept Anat & Cell Biol London ON N6A 5C1 Canada

Using a murine breast cancer model, we earlier found a positive correlation between the expression of nitric oxide synthase (NOS) and tumor progression;treatment with inhibitors of NOS, N(G)-methyl-L-arginine (NMMA) and N(G)-nitro-L-arginine methyl ester (L-NAME), had antitumor and antimetastatic effects that were partly attributed to reduced tumor cell invasiveness. In the present study, we used a novel in vivo model of tumor angiogenesis using subcutaneous implants of tumor cells suspended in growth factor-reduced Matrigel to examine the angiogenic role of NO in a highly metastatic murine mammary adenocarcinoma cell line. This cell line, C3L5, expresses endothelial (e) NOS in vitro and in vivo, and inducible (i) NOS in vitro on stimulation with Lipopolysaccharide and interferon-gamma. Female C3H/HeJ mice received subcutaneous implants of growth factor-reduced Matrigel inclusive of C3L5 cells on one side, and on the contralateral side, Matrigel alone;L-NAME and D-NAME (inactive enantiomer) were subsequently administered for 14 days using osmotic minipumps, Immediately after sacrifice, implants were removed and processed for immunolocalization of eNOS and NOS proteins, and measurement of angiogenesis, Neovascularization was quantified in sections stained with Masson's trichrome or immunostained for the endothelial cell specific CD31 antigen. While most tumor cells and endothelial cells expressed immunoreactive eNOS protein, iNOS was localized in endothelial cells and some macrophages within the tumor-inclusive implants. Measurable angiogenesis occurred only in implants containing tumor cells. Irrespective of the method of quantification used, tumor-induced neovascularization was significantly reduced in L-NAME-treated mice relative to those treated with D-NAME, The quantity of stromal tissue was lower, but the quantity of necrotic tissue higher in L-NAME relative to D-NAME-treated animals. The total mass of viable tissue (ie, stroma and tumor cells) was lower in L-N

关键词：抗原 CD31/代谢着色剂疾病模型动物内皮血管/酶学酶抑制剂/治疗应用免疫组织化学巨噬细胞/酶学乳房肿瘤动物/血液供给乳房肿瘤动物/药物疗法乳房肿瘤动物/代谢小鼠近交C3H NG-硝基精氨酸甲酯/治疗应用肿瘤移植新生血管化病理性/药物疗法新生血管化病理性/病理学一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢一氧化氮合酶Ⅱ型一氧化氮合酶Ⅲ型肿瘤细胞培养的动物女(雌)性小鼠

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Antioxidant and inflammatory response after acute nitrogen dioxide and ozone exposures in C57Bl/6 mice

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INHALATION TOXICOLOGY 2000年第3期12卷 187-203页

作者： Johnston, CJ Reed, CK Avissar, NE Gelein, R Finkelstein, JN Univ Rochester Dept Environm Med Rochester NY 14642 USA Univ Rochester Dept Pediat Neonatol Rochester NY 14642 USA Univ Rochester Dept Surg Rochester NY 14642 USA

Ozone (O-3) and nitrogen dioxide (NO2) are highly reactive and toxic oxidant pollutants. The objective of this study is to compare chemokine, cytokine, and antioxidant changes elicited by acute exposures of O-3 and NO2 in a genetically sensitive mouse. Eight-week-old C57BI/6J mice were exposed to 1 or 2.5 ppm ozone or 15 of 30 ppm NO2 for 4 or 24 h. Changes in mRNA abundance in lung were assayed by slot blot and ribonuclease protection assay (RPA). Messages encoding metallothionein (Mt), heme oxygenase 1 (HO-1), and inducible nitric oxide synthase (iNOS) demonstrated increased message abundance after 4 and 24 h of exposure to either O-3 or NO2. Furthermore, increases in message abundance were of a similar magnitude for O-3 and NO2. Messages encoding eotaxin, macrophage inflammatory protein (MIP)-1 alpha, and MIP-2 were elevated after 4 and 24 h of exposure to I ppm ozone. Interleukin-6 was elevated after 4 h of exposure to ozone. After 4 h of 2.5 ppm ozone exposure, increased mRNAs of eotaxin, MIP-1 alpha: MIP-2, Mt, MO-1, and iNOS were elevated to a higher magnitude than were detected after I ppm ozone. Monocyte chemoattractant protein (MCP-1) was elevated following 15 ppm NO2 exposure. After 4 h of 30 ppm NO2 exposure, messages encoding eotaxin, MIP-1 alpha MIP-2, and MCP-I were elevated to levels similar to those detected after ozone exposure. Our results demonstrate a similar antioxidant and chemokine response during both O-3 and NO2 exposure. Induction of these messages is associated with the duration and concentration of exposure. These studies suggest that these gases exert toxic action through a similar mechanism.

关键词：投药吸入空气污染物/毒性趋化因子CCL2/遗传学趋化因子CCL2/代谢炎症趋化因子类/遗传学炎症趋化因子类/代谢趋化因子 CC 细胞因子类/遗传学细胞因子类/代谢血红素氧化酶(脱环)/遗传学血红素氧化酶(脱环)/代谢白细胞介素6/遗传学白细胞介素6/代谢肺/药物作用肺/代谢肺疾病间质性/化学诱导肺疾病间质性/代谢金属硫蛋白/遗传学金属硫蛋白/代谢小鼠近交C57BL 单核细胞激活素/遗传学单核细胞激活素/代谢一氧化氮合酶/遗传学一氧化氮合酶/代谢一氧化氮合酶Ⅱ型二氧化氮/投药和剂量二氧化氮/毒性核酸酶保护测定氧化剂光化学/投药和剂量氧化剂光化学/毒性臭氧/投药和剂量臭氧/毒性 RNA 信使/分析 RNA 信使/代谢动物男(雄)性小鼠

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Inositol phosphate metabolism and nitric-oxide synthase activity in endothelial cells are involved in the vasorelaxant activity of nebivolol

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期292卷 698-703页

作者： Parenti, A Filippi, S Amerini, S Granger, HJ Fazzini, A Ledda, F Univ Florence Dept Preclin & Clin Pharmacol Lab Microvasc & Cardiovasc Pharmacol Florence Italy Texas A&M Univ Syst Hlth Sci Ctr Microcirculat Res Inst College Stn TX USA Texas A&M Univ Syst Hlth Sci Ctr Dept Med Physiol College Stn TX USA

Nebivolol is a recently developed beta-blocker provided with vasodilator properties. Because the mechanism of the putative endothelium-dependent effect of this beta-adrenoceptor blocker has not been completely elucidated, the aim of this study was to investigate the effects of nebivolol on an isolated resistance vascular bed and on cell messengers and constitutive nitric-oxide synthase activity (cNOS) in endothelial cells. Experiments were carried out using the rat mesenteric vascular bed and cultured bovine coronary postcapillary venular endothelial cells from bovine heart (CVEC). In mesenteric vascular bed preconstricted by 30 mu M noradrenaline and 0.3 mu M U46619, dl-nebivolol induced a concentration-dependent relaxing effect at concentrations between 3 and 30 mu M;this effect was changed to a concentration-dependent vasoconstrictor response either in endothelium-denuded preparations or in intact preparations pretreated with 100 mM N-omega-nitro-L-arginine methyl ester plus 3 mu M indomethacin. The vasorelaxant effect of dl-nebivolol in preconstricted preparations was completely blocked by pretreatment either with the phospholipase C inhibitor U73122 (1 mu M) or with the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin (1 mu M) for 30 min. The cellular level of the inositol trisphosphate metabolite inositol monophosphate in coronary postcapillary venular endothelial cells was not affected by dl-nebivolol in the concentration range 100 nM to 1 mu M, but it was concentration dependently increased after exposure for 15 min to 10 and 30 mu M dl-nebivolol. The activity of cNOS was almost doubled after a 5-min exposure to 10 mu M dl-nebivolol and was significantly impaired by thapsigargin and N-omega-nitro-L-arginine methyl ester treatment, although it was unaffected by N-omega-nitro-D-arginine methyl ester. These findings demonstrate that nebivolol, in micromolar concentrations, induces vasorelaxation through activation of inositol phosphate metabolism and st

关键词：苯吡喃类/药理学细胞培养的剂量效应关系药物内皮血管/代谢雌烯类/药理学乙醇胺类/药理学吲哚美辛/药理学肌醇磷酸类/代谢肠系膜动脉/代谢心肌/代谢 NG-硝基精氨酸甲酯/药理学一氧化氮合酶/代谢去甲肾上腺素/药理学吡咯烷酮类/药理学大鼠 Wistar 毒胡萝卜内酯/药理学时间因素血管舒张药/药理学静脉/代谢动物牛大鼠

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Repetitive prenatal glucocorticoids increase lung endothelial nitric oxide synthase expression in ovine fetuses delivered at term

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PEDIATRIC RESEARCH 2000年第1期48卷 75-83页

作者： Grover, TR Ackerman, KG Le Cras, TD Jobe, AH Abman, SH Univ Colorado Sch Med Pediat Heart Lung Ctr Denver CO 80262 USA Univ Colorado Sch Med Dept Pediat Denver CO 80262 USA Childrens Hosp Med Ctr Cincinnati OH 45229 USA

Antenatal administration of glucocorticoids has been shown to improve postnatal lung function after preterm birth in the ovine fetus. Mechanisms of steroid-induced lung maturation include increased surfactant production and altered parenchymal lung structure. Whether steroid treatment also affects lung vascular function is unclear. Because nitric oxide contributes to the fall in pulmonary vascular resistance at birth, we hypothesized that the improvement of postnatal lung function of preterm lambs after treatment with prenatal glucocorticoids may be in part caused by an increase in endothelial nitric oxide synthase (eNOS) activity. To determine whether glucocorticoid treatment increases lung eNOS expression, we measured eNOS protein content by Western blot analysis of distal lung homogenates and immunostaining of formalin-fixed lungs from ovine fetuses delivered at preterm and term gestation after prenatal administration of glucocorticoids. Treatment protocols were followed in which ewes were treated with intramuscular betamethasone (0.5 mg/kg) at single or multiple doses at weekly intervals, and fetuses were delivered at 125, 135, or 145 d gestation. All groups were compared with saline-treated controls. Western blot analysis of whole lung homogenates demonstrated a 4-fold increase in eNOS protein content in lambs treated with repetitive doses of glucocorticoids and delivery at term (145 d;p < 0.002). In addition, a small increase in lung eNOS protein content was seen in lambs treated with a single dose of betamethasone at 128 d gestation with delivery at 135 d gestation. In comparison with control animals, there were no differences in lung eNOS content from the remaining lambs treated with glucocorticoids when delivery occurred at preterm ages (125 and 135 d). Immunostaining showed eNOS predominantly in the vascular endothelium in all vessel sizes. Pattern of staining was not altered by treatment with antenatal glucocorticoids. We conclude that maternal treatment

关键词：动物新生倍他米松/投药和剂量倍他米松/药理学剖宫产术用药计划表孕龄糖皮质激素类/药理学免疫组织化学注射肌肉内肺/药物作用肺/胚胎学肺/酶学一氧化氮合酶/代谢一氧化氮合酶Ⅲ型参考值绵羊动物女(雌)性妊娠

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Proteolytic cleavage confers nitric oxide synthase inducing activity upon prolactin

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JOURNAL OF BIOLOGICAL CHEMISTRY 2000年第18期275卷 13183-13186页

作者： Corbacho, AM Nava, G Eiserich, JP Noris, G Macotela, Y Struman, I de la Escalera, GM Freeman, BA Clapp, C Univ Nacl Autonoma Mexico Ctr Neurobiol Juriquilla Queretaro 76001 Qro Mexico Univ Alabama Birmingham Dept Anesthesiol Birmingham AL 35233 USA Univ Alabama Birmingham Dept Biochem Birmingham AL 35233 USA Univ Alabama Birmingham Dept Mol Genet Birmingham AL 35233 USA Univ Alabama Birmingham Ctr Free Rad Biol Birmingham AL 35233 USA Univ Liege Lab Biol Mol & Genie Genet B-4000 Sart Tilman Par Liege Belgium

Prolactin (PRL), originally associated with milk secretion, is now known to possess a wide variety of biological actions and diverse sites of production beyond the pituitary, Proteolytic cleavage is a common post-translational modification that can either activate precursor proteins or confer upon the peptide fragment unique biological actions not exerted by the parent molecule. Recent studies have demonstrated that the 16-kDa N-terminal proteolytic cleavage product of PRL (16K-PRL) acts as a potent inhibitor of angiogenesis. Despite previous demonstrations of 16K-PRL production in vivo, biological functions beyond its antiangiogenic actions remain unknown. Here we show that 16K-PRL, but not full-length PRL, acts to promote the expression of the inducible isoform of nitric oxide synthase (iNOS) and nitric oxide ((NO)-N-.) production by pulmonary fibroblasts and alveolar type II cells with potency comparable with the proinflammatory cytokines interleukin-1 beta, interferon gamma, and tumor necrosis factor alpha. The differential effect of 16K-PRL versus PRL occurs through a receptor distinct from known PRL receptors. Additionally, pulmonary fibroblasts express the PRL gene and endogenously produce 16K-PRL, suggesting that this pathway may serve both autocrine and paracrine roles in the regulation of (NO)-N-. production. These results reveal that proteolytic cleavage of PRL confers upon this classical hormone potent iNOS inducing activity, suggesting its role in inflammatory/immune processes.

关键词：细胞培养的酶诱导/药物作用成纤维细胞/代谢一氧化氮/代谢一氧化氮合酶/代谢一氧化氮合酶Ⅱ型肽碎片/代谢肽碎片/药理学催乳素/代谢催乳素/药理学大鼠 Sprague-Dawley 动物大鼠

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