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A novel role for erythropoietin during fibrin-induced wound-healing response

AMERICAN JOURNAL OF PATHOLOGY 2003年第3期163卷 993-1000页

作者： Haroon, ZSA Amin, K Jiang, XH Arcasoy, MO Duke Univ Sch Med Dept Med Durham NC 27710 USA SRI Int Biosci Div Menlo Pk CA 94025 USA Synergen Inc San Francisco CA USA

In this study, we investigated the role of the hematopoietic cytokine erythropoietin (EPO) during wound healing, the physiological response to tissue injury. We used an in vivo wound-healing assay (fibrin Z-chambers) consisting of fibrin-filled chambers implanted subcutaneously in rats. The fibrin inside the chambers is replaced by granulation tissue consisting of new blood vessels, macrophages and fibroblasts as part of the wound-healing response. Local, exogenous recombinant EPO administration into the fibrin matrix significantly increased granulation tissue formation in a dose-dependent manner. To investigate the physiological role of endogenous EPO during wound healing, we used soluble EPO receptor or anti-EPO monoclonal antibodies to neutralize EPO and observed dose-dependent inhibition of granulation tissue formation, consistent with an important role for EPO in the wound-healing;cascade. The ability of recombinant EPO to promote wound healing was associated with a proangiogenic effect during granulation tissue formation. We also found abundant expression of EPO receptor protein in macrophages, cells that play a pivotal role during wound healing. Modulation of wound healing because of administration of recombinant EPO or inhibition of endogenous EPO-EPO receptor correlated with changes in levels of inducible nitric oxide synthase protein in granulation tissue. These data demonstrate a novel function for EPO by providing in vivo evidence for a physiological role during fibrin-induced wound healing.

关键词：抗体/药理学红细胞生成素/拮抗剂和抑制剂红细胞生成素/免疫学红细胞生成素/代谢红细胞生成素/药理学纤维蛋白/药理学巨噬细胞/代谢新生血管化生理性一氧化氮合酶/代谢一氧化氮合酶Ⅱ型大鼠近交F344 受体红细胞生成素/拮抗剂和抑制剂受体红细胞生成素/化学受体红细胞生成素/代谢重组蛋白质类/药理学皮肤/损伤皮肤/病理生理学溶解度伤口愈合/药物作用创伤和损伤/代谢创伤和损伤/病理学创伤和损伤/病理生理学动物女(雌)性大鼠

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Nitric oxide and the proliferation of vascular smooth muscle cells

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CARDIOVASCULAR RESEARCH 1999年第3期43卷 580-594页

作者： Jeremy, JY Rowe, D Emsley, AM Newby, AC Bristol Royal Infirm & Gen Hosp Bristol Heart Inst Bristol BS2 8HW Avon England

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Peroxisome proliferator-activated receptor-γ agonists prevent experimental autoimmune encephalomyelitis

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ANNALS OF NEUROLOGY 2002年第6期51卷 694-702页

作者： Feinstein, DL Galea, E Gavrilyuk, V Brosnan, CF Whitacre, CC Dumitrescu-Ozimek, L Landreth, GE Pershadsingh, HA Weinberg, G Heneka, MT Univ Illinois Dept Anesthesiol Chicago IL 60612 USA Albert Einstein Coll Med Dept Pathol Bronx NY 10467 USA Ohio State Univ Dept Mol Virol Immunol & Med Genet Columbus OH 43210 USA Univ Bonn Dept Neurol D-5300 Bonn Germany Case Western Reserve Univ Dept Neurosci Cleveland OH 44106 USA Case Western Reserve Univ Dept Neurol Cleveland OH 44106 USA Univ Calif Irvine Irvine CA USA Kern Med Ctr Dept Family Med Irvine CA USA

The development of clinical symptoms in multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE) involves T-cell activation and migration into the central nervous system, production of glial-derived inflammatory molecules, and demyelination and axonal damage. Ligands of the peroxisome proliferator-activated receptor (PPAR) exert anti-inflammatory effects on glial cells, reduce proliferation and activation of T cells, and induce myelin gene expression. We demonstrate in two models of EAE that orally administered PPAR-gamma ligand pioglitazone reduced the incidence and severity of monophasic, chronic disease in C57BL/6 mice immunized with myelin oligodendrocyte glycoprotein peptide and of relapsing disease in B10.P1 mice immunized with myelin basic protein. Pioglitazone also reduced clinical signs when it was provided after disease onset. Clinical symptoms were reduced by two other PPAR-gamma agonists, suggesting a role for PPARgamma activation in protective effects. The suppression of clinical signs was paralleled by decreased lymphocyte infiltration, lessened demyelination, reduced chemokine and cytokine expression, and increased inhibitor of kappa B (IkB) expression in the brain. Pioglitazone also reduced the antigen-dependent interferon-gamma production from EAE-derived T cells. These results suggest that orally administered PPARgamma agonists could provide therapeutic benefit in demyelinating disease.

关键词：小脑/细胞学小脑/生理学大脑皮质/细胞学大脑皮质/生理学 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/代谢脑脊髓炎自身免疫性实验性/药物疗法脑脊髓炎自身免疫性实验性/免疫学脑脊髓炎自身免疫性实验性/病理学糖蛋白类/投药和剂量糖蛋白类/免疫学降血糖药/治疗应用 I-κB蛋白质类配体淋巴细胞活化小鼠近交C57BL 多发性硬化/免疫学多发性硬化/病理生理学一氧化氮合酶/遗传学一氧化氮合酶/代谢一氧化氮合酶Ⅱ型恶唑类/治疗应用肽碎片/投药和剂量肽碎片/免疫学受体胞质和核/激动剂受体胞质和核/免疫学缓解诱导脊髓/细胞学脊髓/病理学 T淋巴细胞/免疫学 T淋巴细胞/代谢噻唑类/治疗应用噻唑烷二酮类转录因子/激动剂转录因子/免疫学酪氨酸/类似物和衍生物酪氨酸/治疗应用动物女(雌)性人类男(雄)性小鼠

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Inducible nitric oxide synthase expression in human colorectal cancer -: Correlation with tumor angiogenesis

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AMERICAN JOURNAL OF PATHOLOGY 2003年第3期162卷 793-801页

作者： Cianchi, F Cortesini, C Fantappiè, O Messerini, L Schiavone, N Vannacci, A Nistri, S Sardi, I Baroni, G Marzocca, C Perna, F Mazzanti, R Bechi, P Masini, E Univ Florence Sch Med Dept Gen Surg Florence Italy Univ Florence Sch Med Dept Internal Med Florence Italy Univ Florence Sch Med Dept Human Pathol & Oncol Florence Italy Univ Florence Sch Med Dept Expt Pathol & Oncol Florence Italy Univ Florence Sch Med Dept Preclin & Clin Pharmacol Florence Italy Univ Florence Sch Med Dept Anat Histol & Forens Med Florence Italy Univ Florence Sch Med Dept Pediat Oncohematol Unit Florence Italy

To investigate the potential involvement of the nitric oxide (NO) pathway in colorectal carcinogenesis, we correlated the expression and the activity of inducible nitric oxide synthase (iNOS) with the degree of tumor angiogenesis in human colorectal cancer. Tumor samples and adjacent normal mucosa were obtained from 46 surgical specimens. Immunohistochemical expression of iNOS, vascular endothelial growth factor (VEGF), and CD31 was analyzed on paraffin-embedded tissue sections. iNOS activity and cyclic GMP levels were assessed by specific biochemical assays. iNOS protein expression was determined by Western blot analysis. iNOS and VEGF mRNA levels were evaluated using Northern blot analysis. Both iNOS and VEGF expressions correlated significantly with intratumor microvessel density (r(s) = 0.31, P = 0.02 and r(s) = 0.67, P < 0.0001, respectively). A significant correlation was also found between iNOS and VEGF expression (P = 0.001). iNOS activity and cyclic GMP production were significantly higher in the cancer specimens than in the normal mucosa (P < 0.0001 and P < 0.0001, respectively), as well as in metastatic tumors than in nonmetastatic ones (P = 0.002 and P = 0.04, respectively). Western and Northern blot analyses confirmed the up-regulation of the iNOS protein and gene in the tumor specimens as compared with normal mucosa. NO seems to play a role in colorectal. cancer growth by promoting tumor angiogenesis.

关键词：抗原 CD/代谢抗原 CD31/代谢印迹法 RNA 结直肠肿瘤/血液供给结直肠肿瘤/酶学结直肠肿瘤/遗传学结直肠肿瘤/病理学环GMP/代谢地诺前列酮/代谢内皮生长因子/分析内皮生长因子/遗传学免疫组织化学胞间信号肽类和蛋白质类/分析胞间信号肽类和蛋白质类/遗传学淋巴因子/分析淋巴因子/遗传学新生血管化病理性/遗传学新生血管化病理性/病理学一氧化氮合酶/遗传学一氧化氮合酶/代谢一氧化氮合酶Ⅱ型 RNA 信使/遗传学转录遗传血管内皮生长因子A 血管内皮生长因子类人类

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Intimal growth and neovascularization in human stenotic vein grafts

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JOURNAL OF THE AMERICAN COLLEGE OF SURGEONS 2000年第3期191卷 264-271页

作者： Westerband, A Gentile, AT Hunter, GC Gooden, MA Aguirre, ML Berman, SS Mills, JL So Arizona Vet Affairs Hlth Care Syst Sect Vasc Surg 2 112 Tucson AZ 85723 USA Univ Arizona Hlth Sci Ctr Vasc Surg Sect Tucson AZ USA Univ Arizona Hlth Sci Ctr Dept Pathol Tucson AZ USA Univ Texas Med Branch Dept Surg Galveston TX 77550 USA

Background: Myointimal thickening and microvessel ingrowth are commonly observed in vein graft stenosis, which complicates a third of infrainguinal bypass procedures. But a direct correlation between these two features has not been established. Our purpose was to analyze the relationship between neovascularity and intimal thickness in human vein grafts. Study Design: Twenty-two explant stenotic vein grafts (STVG), 8 nonstenotic arterialized vein grafts (AVG), and 20 age-matched control greater saphenous veins (CGSV) were analyzed histologically and compared morphologically by light microscopy. Digitized computer image analysis was used to measure intimal thickness and quantitate microvessel ingrowth. Immunolocalization of endothelial cells around the lumen and in microvessels was determined using antibodies to factor VIII and to endothelial nitric oxide synthase (eNOS), respectively. Results: Focal areas of endothelial disruption and thrombus deposition were present in 23% (5 of 22) of stenotic vein grafts. The neointima of STVG grafts was two- and fourfold thicker than that of AVG and CGSV, respectively (p < 0.0001). Microvessels were most frequently observed in the adventitia and media of STVG and increased in number with increasing intimal thick-ness (p < 0.001 by ANOVA). Conclusions: A fourfold increased neointimal thickness in critically stenotic vein grafts is associated with increased medial and adventitial neovascularization. Remodeling alone with doubling of the intimal thick- ness in nonstenotic arterialized vein grafts does not appear to be associated with enhancement of the graft microvasculature. More specific observations using an experimental model may allow us to further define the role of angiogenesis in vein graft stenosis and to deter- mine the therapeutic implications of such observations.

关键词：人工血管缩窄病理性内皮血管/细胞学内皮血管/病理学免疫组织化学间歇性跛行/病理学缺血/病理学缺血/外科学小腿/血液供给新生血管化病理性一氧化氮合酶/代谢一氧化氮合酶Ⅲ型血管内膜/病理学静脉/病理学老年人老年人 80以上女(雌)性人类男(雄)性中年人

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α-MSH peptides inhibit production of nitric oxide and tumor necrosis factor-α by microglial cells activated with β-amyloid and interferon γ

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第1期263卷 251-256页

作者： Galimberti, D Baron, P Meda, L Prat, E Scarpini, E Delgado, R Catania, A Lipton, JM Scarlato, G Univ Milan IRCCS Osped Maggiore Policlin Inst NeurolDino Ferrari Ctr I-20122 Milan Italy Univ Milan IRCCS Osped Maggiore Policlin Div Internal Med 3 I-20122 Milan Italy Univ Texas SW Med Ctr Dept Physiol Dallas TX 75235 USA Univ Texas SW Med Ctr Dept Anesthesiol Dallas TX 75235 USA

alpha-Melanocyte stimulating hormone (alpha-MSH) is an ancient tridecapeptide with potent inhibitory activity in all major forms of inflammation. The anti-inflammatory message sequence of alpha-MSH resides in the COOH-terminal tripeptide alpha-MSH[11-13]. We tested the influence of alpha-MSH[1-13] and of alpha-MSH[11-13] in a cultured murine microglia cell line known to produce nitric oxide (NO2-) and tumor necrosis factor (TNF alpha) when stimulated with beta-amyloid protein (A beta). Melanocortin peptides significantly inhibited release of both NO2- and TNF alpha into cell-free supernatants from microglia stimulated with A beta[1-42] or A beta[25-35] peptides and interferon gamma (IFN gamma). Northern blot analysis demonstrated that alpha-MSH[1-13] and alpha-MSH[11-13] inhibited accumulation of inducible nitric oxide synthase (iNOS) and TNF alpha mRNA was triggered by A beta stimulation. A beta/microglial interaction is believed to promote the progression of inflammatory and neurodegenerative changes in senile plaques in Alzheimer's disease. Our data indicate that alpha-MSH peptides might be used to modulate the local response of the brain to A beta deposition in this neurodegenerative disease. (C) 1999 Academic Press.

关键词：细胞系炎症介导素类/代谢黑素细胞刺激激素类/药理学小神经胶质细胞/药物作用小神经胶质细胞/代谢一氧化氮/生物合成一氧化氮合酶/遗传学一氧化氮合酶/代谢一氧化氮合酶Ⅱ型肽碎片/药理学 RNA 信使/遗传学 RNA 信使/代谢重组蛋白质类肿瘤坏死因子α/生物合成肿瘤坏死因子α/遗传学 α促黑素/药理学动物小鼠

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VEGF induces nuclear translocation of Flk-1/KDR, endothelial nitric oxide synthase, and caveolin-1 in vascular endothelial cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第1期256卷 192-197页

作者： Feng, YY Venema, VJ Venema, RC Tsai, N Caldwell, RB Med Coll Georgia Dept Anat & Cellular Biol Augusta GA 30912 USA Med Coll Georgia Vasc Biol Ctr Augusta GA 30912 USA Med Coll Georgia Dept Ophthalmol Augusta GA 30912 USA Med Coll Georgia Dept Pediat Augusta GA 30912 USA

VEGF increases endothelial cell permeability and growth by a process requiring NOS activity. Because eNOS activity is regulated by its interaction with the caveolar structural protein caveolin-1, we analyzed VEGF effects on structural interactions between eNOS, caveolin-1 and the VEGF receptor Flk-1/KDR. Confocal immunolocalization analysis of the subcellular distribution of Flk-1/KDR, caveolin-1 and eNOS showed that VEGF stimulated the translocation of all three proteins into the nucleus. This result was confirmed by cell fractionation and immunoblotting studies showing that levels of all three proteins within the caveolar compartment declined progressively after 30 and 60 min of VEGF treatment. The pattern was reversed for nuclear fractions. Protein levels were lowest in the control cultures, but increased progressively after 30 and 60 min of treatment. Nuclear translocation of eNOS and Flk-1/KDR within caveolae may represent a mechanism for targeting NO production to the nuclear compartment where it could influence transcription factor activation. (C) 1999 Academic Press.

关键词：主动脉印迹法蛋白质窖蛋白1 细胞质膜微囊蛋白细胞分级分离细胞核/药物作用细胞核/代谢细胞培养的内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用内皮血管/代谢免疫组织化学淋巴因子/药理学膜蛋白质类/代谢一氧化氮合酶/代谢一氧化氮合酶Ⅲ型受体蛋白质酪氨酸激酶类/代谢受体生长因子/代谢受体血管内皮生长因子视网膜信号传导/药物作用时间因素血管内皮生长因子A 血管内皮生长因子类动物牛

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Production of prostanoids and nitric oxide by infarcted heart in situ and the effect of aspirin

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第2期257卷 488-493页

作者： Yamamoto, T Cohen, AM Kakar, NR Yamamoto, M Johnson, PE Cho, YK Bing, RJ Huntington Med Res Inst Dept Expt Cardiol Pasadena CA 91101 USA

The production of prostacyclin (PGI(2)) and thromboxane A(2) (TXA(2)) in infarcted and noninfarcted portions of the rabbit heart was studied prior to and following administration of acetylsalicylic acid (aspirin). Aspirin was administered intravenously (iv) as water-soluble Aspisol, D-lysinmono (acetylsalicylate) (Bayer, Leverkusen, Germany) into an ear vein. A branch of the left circumflex coronary artery was ligated. The animals were divided into three groups. The first group received 150 mg/kg/day of aspirin (75 mg/kg of aspirin every 12 h, n = 10). The first administration of aspirin was 1 h after ligation of the coronary artery and the last injection was 1 h before euthanasia. The second group received 5 mg/kg/day of aspirin (every 24 h, n = 10). A separate group of rabbits not receiving aspirin served as controls (n = 12). Two days following onset of ischemia, inducible form of nitric oxide synthase (iNOS) was measured in heart muscle and the oxidation products of nitric oxide (nitrite, NO2- plus nitrate, NO3-: their sum referred to as NOx) were determined in arterial and coronary venous blood. Concentrations of both PGI(2) and TXA(2) were elevated in the infarcted portions of the heart compared to the noninfarcted regions. Formation of prostanoids was accompanied by increased activation of iNOS. Both doses of aspirin diminished the concentrations of PGI(2) and TXA(2) in infarcted heart muscle;in contrast, small doses of aspirin failed to influence myocardial iNOS activity. Apparently small doses of aspirin changed the relationship of iNOS to cyclooxygenase (COX). Coronary arterial-venous difference of NOx and myocardial iNOS activity showed parallel increases. Diminution of prostacyclin by aspirin can damage gastric mucosa and interfere with vasodilatation. Since NO counters these deficiencies, a combination of aspirin with a nitric oxide donor may be advantageous. (C) 1999 Academic Press.

关键词： 6-酮前列腺素F1α/代谢阿司匹林/药理学冠状血管/药物作用冠状血管/代谢酶激活/药物作用依前列醇/生物合成心脏/药物作用心肌梗死/酶学心肌梗死/代谢心肌/酶学心肌/代谢硝酸盐类/代谢一氧化氮/代谢一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/代谢一氧化氮合酶Ⅱ型亚硝酸盐类/代谢前列腺素/代谢血栓烷A2/生物合成血栓烷B2/代谢动物兔

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Role of nitric oxide in the pathogenesis of chronic pulmonary hypertension

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PHYSIOLOGICAL REVIEWS 2000年第4期80卷 1337-1372页

作者： Hampl, V Herget, J Charles Univ Prague Sch Med 2 Dept Physiol Prague 15000 5 Motol Czech Republic

Chronic pulmonary hypertension is a serious complication of a number of chronic lung and heart diseases. In addition to vasoconstriction, its pathogenesis includes injury to the peripheral pulmonary arteries leading to their structural remodeling. Increased pulmonary vascular synthesis of an endogenous vasodilator, nitric oxide (NO), opposes excessive increases of intravascular pressure during acute pulmonary vasoconstriction and chronic pulmonary hypertension, although evidence for reduced NO activity in pulmonary hypertension has also been presented. NO can modulate the degree of vascular injury and subsequent fibroproduction, which both underlie the development of chronic pulmonary hypertension. On one hand, NO can interrupt vascular wall injury by oxygen radicals produced in increased amounts in pulmonary hypertension. NO can also inhibit pulmonary vascular smooth muscle and fibroblast proliferative response to the injury. On the other hand, NO may combine with oxygen radicals to yield peroxynitrite and other related, highly reactive compounds. The oxidants formed in this manner may exert cytotoxic and collagenolytic effects and, therefore, promote the process of reparative vascular remodeling. The balance between the protective and adverse effects of NO is determined by the relative amounts of NO and reactive oxygen species. We speculate that this balance may be shifted toward more severe injury especially during exacerbations of chronic diseases associated with pulmonary hypertension. Targeting these adverse effects of NO-derived radicals on vascular structure represents a potential novel therapeutic approach to pulmonary hypertension in chronic lung diseases.

关键词：慢性病内皮血管/药物作用内皮血管/代谢酶抑制剂/药理学自由基/代谢自由基/药理学高血压肺性/病因学高血压肺性/代谢肺/血液供给肺/药物作用肺/胚胎学一氧化氮/代谢一氧化氮/药理学一氧化氮合酶/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型肺循环/药物作用肺循环/生理学血管阻力/药物作用血管阻力/生理学血管收缩/药物作用血管收缩/生理学血管舒张/药物作用血管舒张/生理学成年人动物人类婴儿新生

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Modulation of nitric-oxide synthase by nicotine

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第2期295卷 601-606页

作者： Tonnessen, BH Severson, SR Hurt, RD Miller, VM Mayo Clin & Mayo Fdn Dept Surg Rochester MN 55905 USA Mayo Clin & Mayo Fdn Dept Internal Med Rochester MN 55905 USA Mayo Clin & Mayo Fdn Nicotine Res Ctr Rochester MN 55905 USA Mayo Clin & Mayo Fdn Dept Physiol & Biophys Rochester MN 55905 USA

Effects of nicotine on arterial endothelium-dependent relaxations mediated by nitric oxide are controversial. Experiments were designed to test the hypothesis that nicotine can directly alter activity of endothelial nitric-oxide synthase (eNOS). NOS from aortic endothelial cells of untreated dogs and recombinant eNOS, neuronal NOS, and inducible NOS were used for these experiments. NOS activity was determined as conversion of L-[H-3] arginine to L-[H-3] citrulline in the absence or presence of nicotine (10(-7)-10(-3) M) in vitro. In separate assays, concentrations of cofactors NADPH, FAD, and tetrahydrobioprotein were reduced by half to assess for possible interaction with nicotine. With enzyme from aortic endothelial cells, total and calcium-dependent accumulation of citrulline increased by 30% in the presence of 10(-5) M nicotine. Nicotine dose dependently also increased citrulline accumulation by recombinant eNOS and neuronal NOS but not inducible NOS. Effects of nicotine on accumulation of citrulline by isolated eNOS and recombinant eNOS were further modulated by changes in the concentration of NADPH in the incubation solution. Our data demonstrate a significant effect of nicotine on eNOS-mediated citrulline accumulation. These results suggest that effects of nicotine on production of nitric oxide may depend on NADPH or oxygen radical interactions with NOS and thus may explain, in part, inconsistent findings of changes in production of endothelium-derived nitric oxide with nicotine administration.

关键词：主动脉胸/酶学精氨酸/代谢生物蝶呤/类似物和衍生物生物蝶呤/代谢生物蝶呤/药理学瓜氨酸/代谢内皮血管/酶学黄素腺嘌呤二核苷酸/代谢黄素腺嘌呤二核苷酸/药理学 NADP/代谢 NADP/药理学尼古丁/药理学一氧化氮合酶/分离和提纯一氧化氮合酶/代谢一氧化氮合酶Ⅰ型一氧化氮合酶Ⅱ型一氧化氮合酶Ⅲ型重组蛋白质类/代谢动物狗男(雄)性

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