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Chemotactic effect of urokinase plasminogen activator: A major role for mechanisms independent of its proteolytic or growth factor domains

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JOURNAL OF RECEPTOR AND SIGNAL TRANSDUCTION RESEARCH 1999年第6期19卷 939-951页

作者： Poliakov, AA Mukhina, SA Traktouev, DO Bibilashvily, RS Gursky, YG Minashkin, MM Stepanova, VV Tkachuk, VA Moscow State Univ Sch Basic Med Dept Biol & Med Chem Moscow 119899 Russia Cardiol Res Ctr Inst Expt Cardiol Moscow 121552 Russia

Urokinase type plasminogen activator (uPA) converts plasminogen to plasmin and is highly chemotactic for many cell types. We examined, using recombinant wild type and mutated forms of uPA, the extent to which its proteolytic properties, its growth-like domain (GFD) and/or interactions with the specific receptor (uPAR) contribute to the chemotactic activity towards vascular smooth muscle cells (SMC). Recombinant wild type uPA (r-uPA) stimulated cell migration nearly 5.8-fold, inactive r-uPA, with a mutation in the catalitic domain (r-uPA(H/Q)), 3-fold, uPA without growth factor like domain (r-uPA(GFD(-))), 2.6-fold, and a form containing both mutations (r-uPA(H/Q, GFD(-)), 3.3-fold. All recombinant forms of uPA, wild type and those with mutations were equally and highly effective (IC(50)similar to 20 nM) in displacing I-125-r-uPA bound to SMC. These results indicate that additional mechanisms, not dependent on uPA's proteolytic activity or the binding ability of its GFD to uPAR, are the major contributors to its chemotactic action on SMC.

关键词：结合部位/遗传学结合竞争性细胞运动/药物作用细胞培养的趋化作用/药物作用肌平滑血管/药物作用肌平滑血管/病理学突变受体细胞表面/代谢重组蛋白质类/化学重组蛋白质类/遗传学重组蛋白质类/药理学尿纤溶酶原激活物/化学尿纤溶酶原激活物/遗传学尿纤溶酶原激活物/药理学动物大鼠

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Vascular smooth muscle cell proliferation and regrowth after mechanical injury in vitro are Egr-1/NGFI-A-dependent

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AMERICAN JOURNAL OF PATHOLOGY 1999年第3期155卷 897-905页

作者： Santiago, FS Atkins, DG Khachigian, LM Univ New S Wales Sch Pathol Ctr Thrombosis & Vasc Res Sch Pathol Sydney NSW 2052 Australia Johnson & Johnson Res Pty Ltd Sydney NSW Australia

Smooth muscle cell (SMC) proliferation is a key event in renarrowing of blood vessels after balloon angioplasty. Mechanical injury imparted to the arterial wall in experimental models induces the expression of the immediate-early gene, egr-1. Egr-1 binds to and activates expression from the proximal promoters of multiple genes whose products can, in turn, influence the vascular response to injury. Here, we used antisense strategies in vitro to inhibit rat vascular SMC proliferation by directly targeting Egr-1, A series of phosphorothioate antisense oligonucleotides of 15 base length and complementary to various theoretically accessible regions within Egr-1 mRNA were synthesized and assessed for their ability to selectively inhibit SMC proliferation in an Egr-1-dependent manner. Western blot analysis revealed that two oligonucleotides, AS2 and E11, inhibited Egr-1 synthesis in cells exposed to serum without affecting levels of the zinc finger protein Spl. AS2 and E11 inhibited serum-inducible [H-3]thymidine incorporation into DNA, as well as serum stimulation of total cell numbers. Size-matched phosphorothioate oligonucleotides with random, scrambled, sense or mismatch sequences failed to inhibit. Antisense Egr-1 inhibition was nontoxic and reversible. These oligonucleotides also inhibited SMC regrowth after mechanical injury in vitro. Egr-1 thus plays a key regulatory role in SMC proliferation and repair following injury.

关键词：结合部位血蛋白质类/药理学印迹法蛋白质细胞分裂/药物作用细胞培养的 DNA结合蛋白质类/拮抗剂和抑制剂 DNA结合蛋白质类/遗传学 DNA结合蛋白质类/生理学早期生长反应蛋白质1 荧光素-5-异硫氰酸盐基因表达/药物作用即早蛋白质类显微镜检查荧光肌平滑血管/细胞学肌平滑血管/药物作用肌平滑血管/损伤肌平滑血管/代谢核酸构象核酸合成抑制剂/药理学寡核苷酸类反义/代谢寡核苷酸类反义/药代动力学磷放射性同位素血小板源性生长因子/生物合成 RNA 信使/药物作用硫代核苷酸类/药代动力学硫代核苷酸类/药理学时间因素转录因子/拮抗剂和抑制剂转录因子/遗传学转录因子/生理学动物大鼠

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Transdermal nicotine mimics the smoking-induced endothelial dysfunction

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CLINICAL PHARMACOLOGY & THERAPEUTICS 2000年第2期68卷 167-174页

作者： Sabha, M Tanus-Santos, JE Toledo, JCY Cittadino, M Rocha, JC Moreno, H Univ Estadual Campinas Fac Med Sci Dept Pharmacol BR-13081970 Campinas SP Brazil Univ Estadual Campinas Fac Med Sci Dept Med BR-13081970 Campinas SP Brazil

Background: Cigarette smoking is a major risk factor for coronary artery disease and causes endothelial dysfunction, perhaps by decreasing the availability of nitric oxide availability in arteries and veins. Nicotine in cigarette smoke may be responsible for this impaired endothelial response. Methods: We studied nine healthy nonsmokers and 12 healthy mild to moderate smokers by use of the dorsal hand vein compliance technique. Dose-response curves to bradykinin and sodium nitroprusside were obtained to test the endothelium-dependent and endothelium-independent vasorelaxation before and during the use of a nicotine (21 mg) patch. Mean arterial blood pressure and heart rate were measured beat-to-beat during the 4-hour study and serial blood samples were drawn to assay plasma thromboxane B-2 levels. Results: Transdermal nicotine reduced the venous responsiveness to bradykinin in nonsmokers (E-max = 88.0% +/- 17.9% and 54.3% +/- 14.9%, respectively, before and after the nicotine patch;P <.05);the latter response was similar to that in smokers (E-max = 56.3% +/- 16.6%). Sodium nitroprusside-induced venodilation was unaltered. Mean arterial blood pressure increased in both smokers and nonsmokers. Transdermal nicotine increased the plasma thromboxane B-2 concentrations only among nonsmokers, Conclusion: These findings indicate that nicotine can have a major role in the impaired endothelial function in smokers. The results probably also reflect what occurs in arterial beds because the nicotine patches increased the mean arterial blood pressure in both smokers and nonsmokers.

关键词：投药皮肤血压/药物作用缓激肽/药理学交叉研究药物相互作用内皮血管/药物作用内皮血管/生理学心率/药物作用尼古丁/药理学烟碱激动剂/药理学硝普钠/药理学吸烟/血液吸烟/病理学吸烟/病理生理学血栓烷B2/血液血管舒张/药物作用成年人女(雌)性人类男(雄)性

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Endocannabinoids and vascular function

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第1期294卷 27-32页

作者： Hillard, CJ Med Coll Wisconsin Dept Pharmacol & Toxicol Milwaukee WI 53226 USA

Marijuana is used by humans for its psychoactive and medicinal effects. The active constituents of marijuana, the cannabinoids, exert effects via a G protein-coupled receptor, CB1. Two arachidonic acid analogs, N-arachidonylethanolamine and 2-arachidonylglycerol are hypothesized to function as endogenous ligands of the CB1 receptor. The cannabinoids exert significant vascular effects in humans and laboratory animals. In particular, the cannabinoids produce vasodilation and hypotension. The possible mechanisms for these effects are inhibition of transmitter release from sympathetic nerve terminals, direct effects on vascular smooth muscle cells, and effects on endothelial cell function. The data regarding these effects of the cannabinoids and possible sources of endocannabinoid ligands in the vasculature are the subjects of this review.

关键词：花生四烯酸类/药理学内源性大麻酚类内皮血管/药物作用内皮血管/生理学甘油酯类/药理学肌平滑血管/药物作用肌平滑血管/生理学神经元传入/药物作用多不饱和脂肪酸酰胺类受体大麻酚受体药物/药物作用四氢大麻酚/药理学动物人类

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An endothelium-derived hyperpolarizing factor distinct from NO and prostacyclin is a major endothelium-dependent vasodilator in resistance vessels of wild-type and endothelial NO synthase knockout mice

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第17期97卷 9747-9752页

作者： Brandes, RP Schmitz-Winnenthal, FH Félétou, M Gödecke, A Huang, PL Vanhoutte, PM Fleming, I Busse, R Univ Frankfurt Klinikum Inst Kardiovask Physiol D-60590 Frankfurt Germany Inst Rech Servier F-92150 Suresnes France Univ Dusseldorf Inst Herz & Kreislaufphysiol D-40225 Dusseldorf Germany Massachusetts Gen Hosp Cardiovasc Res Ctr Charlestown MA 02129 USA

In addition to nitric oxide (NO) and prostacyclin (PGl(2)) the endothelium generates the endothelium-derived hyperpolarizing factor (EDHF). We set out to determine whether an EDHF-like response can be detected in wild-type (WT) and endothelial NO synthase knockout mice (eNOS -/-) mice. Vasodilator responses to endothelium-dependent agonists were determined in vivo and in vitro. In vivo, bradykinin induced a pronounced, dose-dependent decrease in mean arterial pressure (MAP) which did not differ between WT and eNOS -/- mice and was unaffected by treatment with N-omega-nitro-L-arginine methyl ester and diclofenac. In the saline-perfuse hindlimb of WT and eNOS -/- mice, marked N-omega-nitro-L-arginine (L-NA, 300 mu mol/liter)- and diclofenac-insensitive vasodilations in response to both bradykinin and acetylcholine (ACh) were observed, which were more pronounced than the agonistinduced vasodilation in the hindlimb of WT in the absence of L-NA. This endothelium-dependent, NO/PGl(2)-independent vasodilatation was sensitive to KCl (40 mM) and to the combination of apamin and charybdotoxin. Cap junction inhibitors (18 alpha-glycyrrhetinic acid, octanol, heptanol) and CB-1 cannabinoid-receptor agonists (Delta 9-tetrahydrocannabinol, HU210) impaired EDHF-mediated vasodilation, whereas inhibition of cytochrome P450 enzymes, soluble guanylyl cyclase, or adenosine receptors had no effect on EDHF-mediated responses. These results demonstrate that in murine resistance vessels the predominant agonist-induced endothelium-dependent vasodilation in vivo and in vitro is not mediated by NO, PGl(2), or a cytochrome P450 metabolite, but by an EDHF-like principle that requires functional gap junctions.

关键词：乙酰胆碱/药理学动脉/药物作用动脉/生理学生物因子/代谢血压/药物作用缓激肽/药理学细胞色素P450酶系统/代谢二氯酚酸/药理学内皮血管/药物作用内皮血管/酶学内皮血管/代谢依前列醇/代谢缝隙接合部/药物作用缝隙接合部/生理学基因缺失后肢/血液供给后肢/药物作用小鼠近交C57BL 小鼠基因敲除 NG-硝基精氨酸甲酯/药理学一氧化氮/代谢一氧化氮合酶/拮抗剂和抑制剂一氧化氮合酶/缺乏一氧化氮合酶/遗传学一氧化氮合酶/代谢硝基精氨酸/药理学硝普钠/药理学灌流钾通道阻滞剂钾通道/代谢受体大麻酚受体药物/拮抗剂和抑制剂受体药物/代谢血管舒张/药物作用血管舒张药/代谢血管舒张药/药理学动物小鼠

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Hepatocyte growth factor enhances vascular endothelial growth factor-induced angiogenesis in vitro and in vivo

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AMERICAN JOURNAL OF PATHOLOGY 2001年第3期158卷 1111-1120页

作者： Xin, XH Yang, SY Ingle, G Zlot, C Rangell, L Kowalski, J Schwall, R Ferrara, N Gerritsen, ME Genentech Inc Dept Cardiovasc Res S San Francisco CA 94080 USA Genentech Inc Dept Mol Oncol S San Francisco CA 94080 USA Genentech Inc Dept Pharmacol Sci S San Francisco CA 94080 USA

Vascular endothelial growth factor (VEGF) is an important mediator of angiogenesis in both physiological and pathological processes. Hepatocyte growth factor (HGF) is a mesenchyme-derived mitogen that also stimulates cell migration, and branching and/or tubular morphogenesis of epithelial and endothelial cells. In the present study, we tested the hypothesis that simultaneous administration of HGF and VEGF would synergistically promote new blood vessel formation. HGF acted in concert with VEGF to promote human endothelial cell survival and tubulogenesis in 3-D type I collagen gels, a response that did not occur with either growth factor alone. The synergistic effects of VEGF and HGF on endothelial survival correlated with greatly augmented mRNA levels for the anti-apoptotic genes Bcl-2 and A1. Go-culture experiments with human neonatal dermal fibroblasts and human umbilical vein endothelial cells demonstrated that neonatal dermal fibroblasts, in combination with VEGF, stimulated human umbilical vein endothelial cells tubulogenesis through the paracrine secretion of HGF. Finally, in vivo experiments demonstrated that the combination of HGF and VEGF increased neovascularization in the rat corneal assay greater than either growth factor alone. We suggest that combination therapy using HGF and VEGF co-administration may provide a more effective strategy to achieve therapeutic angiogenesis.

关键词：细胞培养技术/方法细胞系细胞存活/药物作用胶原/生理学角膜/血液供给角膜/药物作用药物协同作用内皮生长因子/药理学内皮血管/细胞学内皮血管/药物作用成纤维细胞/生理学肝细胞生长因子/药理学淋巴因子/药理学新生血管化生理性/药物作用大鼠 Sprague-Dawley 血管内皮生长因子A 血管内皮生长因子类动物人类男(雄)性大鼠

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Fibroblast growth factors are translocated to the nucleus of human endothelial cells in a microtubule- and lysosome-independent pathway

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2000年第2期273卷 551-556页

作者： Hu, GF Kim, HJ Xu, CJ Riordan, JF Harvard Univ Sch Med Ctr Biochem & Biophys Sci & Med Boston MA 02115 USA Harvard Univ Sch Med Dept Radiol Boston MA 02115 USA

Exogenous acidic and basic fibroblast growth factors undergo rapid nuclear translocation in human umbilical vein endothelial cells. When nuclear translocation reaches saturation, more than 70% of the internalized growth factors are in the nuclear fraction. Lysosomal inhibitors, such as leupeptin and chloroquine, and microtubule inhibitors including colchicine and 2-methoxyl-beta-estradiol neither increase nor decrease nuclear translocation. The results suggest that nuclear translocation of fibroblast growth factors does not require cytosolic accumulation or lysosomal processing and that the transportation of exogenous growth factors across the cytoplasm is independent of microtubules. (C) 2000 Academic Press.

关键词：生物转运主动细胞核/代谢细胞培养的氯喹/药理学秋水仙碱/药理学胞质溶胶/代谢内皮血管/药物作用内皮血管/代谢成纤维细胞生长因子1/代谢成纤维细胞生长因子2/代谢成纤维细胞生长因子/代谢动力学亮肽菌素类/药理学溶酶体/药物作用溶酶体/代谢微管/药物作用微管/代谢亚细胞部分/代谢人类

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Endothelium-dependent vasodilatation mechanisms by histamine in simian but not in canine femoral arterial branches

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JOURNAL OF AUTONOMIC PHARMACOLOGY 1999年第5期19卷 267-273页

作者： Arai, M Chiba, S Shinshu Univ Sch Med Dept Pharmacol Matsumoto Nagano 3908621 Japan Shinshu Univ Sch Med Dept Surg 1 Matsumoto Nagano 3908621 Japan

1 The vascular response of isolated, perfused canine and simian femoral arteries, which distribute blood to deep skeletal muscles, were investigated. 2 The vascular responses to histamine, 2-pyridylethylamine (2-PEA), dimaprit and alpha-methylhistamine were pharmacologically analyzed in canine and simian vessels, using diphenhydramine (DPH, a histamine H-1 receptor antagonist), cimetidine (a histamine H-2 antagonist) and saponin which readily removed the endothelium. 3 In canine arteries, alpha-methylhistamine showed no vascular response, but in simian preparations, it caused a slight vasoconstriction. 4 In canine arteries, histamine and 2-PEA consistently induced a vasoconstriction in preconstricted and non-preconstricted preparations. However, in simian arteries histamine usually produced a vasodilatation at small doses (less than 10(-7) mol) and a vasoconstriction at large doses in preconstricted preparations. 5 Vasoconstrictor responses to histamine and 2-PEA were significantly inhibited by DPH in both species. In simian vessels, histamine-and dimaprit-induced vasodilatations were significantly inhibited by cimetidine. 6 After removal of the endothelium by intraluminal treatment with saponin in canine femoral arteries, the vascular responses to histamine, 2-PEA and dimaprit were not significantly affected. On the other hand, in simian femoral arteries, the vasodilatation responses to histamine and 2-PEA were significantly depressed by the removal of endothelium. 7 It is concluded that (1) in both simian and canine femoral arterial branches, there are abundant histamine H-1 and H-2 receptors (2) in simian but not in canine arteries, there exist histamine H-3 receptors, although their role is not clear (3) histamine induces a vasoconstriction mediated via histamine H-1 receptors and a vasodilatation via H-2 receptors which exist in vascular smooth muscle, and (4) in simian but not in canine arteries, there are endothelium-dependent vasodilatation mechanisms.

关键词： Dimaprit/药理学苯海拉明/药理学剂量效应关系药物药物相互作用内皮血管/药物作用内皮血管/生理学股动脉/药物作用组胺/药理学组胺激动药/药理学组胺H1拮抗剂/药理学猕猴属肌平滑血管/药物作用吡啶类/拮抗剂和抑制剂吡啶类/药理学皂苷类/药理学种特异性血管收缩/药物作用血管舒张/药物作用动物狗女(雌)性男(雄)性

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Precontraction with elevated concentrations of extracellular potassium enables both 5-HT_1B and 5-HT_2A "silent" receptors in rabbit ear artery

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期289卷 354-360页

作者： Smith, JR Kim, C Kim, H Purdy, RE Univ Calif Irvine Coll Med Dept Pharmacol Irvine CA 92697 USA

The present study was conducted to determine the effect of a small (<10%) K+-induced precontraction on the response to vasoconstrictors in the rabbit aorta and ear artery rings. in both tissues, 15 mM K+ shifted the methoxamine concentration response curve (CRC) approximately 2.4-fold to the left. There was no change in the sensitivity of the control and amplified CRCs to the alpha(1) adrenoceptor antagonist prazosin (100 nM). In the aorta, the CRC for serotonin was shifted 4.5-fold to the left in the presence of 15 mM K+, and both the control and amplified CRCs were antagonized equally by the 5-HT2A antagonist ketanserin (10 nM). In contrast, 16 and 20 mM K+ caused up to an approximately 60-fold leftward shift of the serotonin CRC in the rabbit ear artery. This effect of 16 mM K+ was not altered by mechanical removal of the endothelium or by in vitro denervation using 6-hydroxydopamine. The K+-amplified CRC was insensitive to 100 nM prazosin al-serotonin concentrations below 3 mu M, but was significantly antagonized by 10 nM ketanserin, suggesting that 5-HT2A receptors are involved in the K+-amplified response. The 5-HT1B-selective antagonist, GR 127935, did not affect control responses to serotonin, but significantly blocked the K+-amplified response. Furthermore, the combination of ketanserin and GR 127935 produced a significantly greater blockade of the amplified response than either antagonist alone, supporting the conclusion that both 5-HT2A and 5-HT1B receptors mediate the K+-amplified response to serotonin in the rabbit ear artery.

关键词：主动脉胸/药物作用主动脉胸/神经支配主动脉胸/代谢主动脉胸/生理学动脉/药物作用动脉/神经支配动脉/代谢动脉/生理学外耳/血液供给外耳/神经支配外耳/代谢肌收缩/药物作用肌收缩/生理学肌平滑血管/药物作用肌平滑血管/神经支配肌平滑血管/代谢肌平滑血管/生理学钾/药理学受体血清素 5-HT1B 受体血清素 5-HT2A 受体血清素/药物作用受体血清素/代谢局部血流/药物作用局部血流/生理学血清素/代谢血清素激动药/药理学血清素拮抗药/药理学交感神经切除术化学血管收缩药/药理学动物男(雄)性兔

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Nicotine regulates basic fibroblastic growth factor and transforming growth factorβ₁ production in endothelial cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第2期257卷 306-312页

作者： Cucina, A Corvino, V Sapienza, P Borrelli, V Lucarelli, M Scarpa, S Strom, R Santoro-D'Angelo, L Cavallaro, A Univ Rome La Sapienza Dept Surg 1 Rome Italy Univ Rome La Sapienza Dept Cellular Biotechnol & Hematol Rome Italy Univ Rome La Sapienza Dept Med Histol & Embryol Rome Italy

Nicotine, a constituent of cigarette smoking, may induce atherosclerosis through the production of growth factors. The pattern of bFGF and TGF beta(1) production and release by bovine aortic endothelial cells (EC) stimulated with nicotine (from 6 x 10(-4) to 6 x 10(-8) M) was studied. EC viability and count were assessed. The presence of bFGF and TGF beta(1) in serum-free conditioned media was determined by the inhibition antibody-binding assay and Western blot analysis. Mitogenic activity of nicotine on EC was also determined. Polymerase chain reaction (PCR) was used to study the expression of bFGF and TGF beta(1). The bFGF release after nicotine stimulation was greater than controls, whereas TGF beta(1) release was lower. At a nicotine concentration of 6 x 10(-6) M we noted the greatest mitogenic activity. The addition of monoclonal antibody anti-bFGF decreased the tritiated thymidine uptake of EC exposed to nicotine but the addition of monoclonal antibody anti-TGF beta(1) had no significant effect, bFGF mRNA expression was significantly higher in EC exposed to nicotine than in controls, whereas TGF beta(1) mRNA expression was not modified. From these data we concluded that nicotine regulates bFGF production and release and TGF beta(1) release and may have a key role in the development and progression of atherosclerosis. (C) 1999 Academic Press.

关键词：抗体单克隆/药理学主动脉动脉硬化/病因学动脉硬化/代谢印迹法蛋白质细胞计数/药物作用细胞分裂/药物作用细胞存活/药物作用培养基条件性/药理学 DNA/生物合成剂量效应关系药物内皮血管/细胞学内皮血管/药物作用内皮血管/代谢内皮血管/病理学成纤维细胞生长因子2/遗传学成纤维细胞生长因子2/免疫学成纤维细胞生长因子2/代谢有丝分裂原/代谢有丝分裂原/药理学肌平滑/细胞学肌平滑/药物作用尼古丁/药理学尼古丁/毒性聚合酶链反应 RNA 信使/代谢转化生长因子β/遗传学转化生长因子β/免疫学转化生长因子β/代谢动物牛

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