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Amoxycillin/clavulanic acid combinations increase transmigration of leucocytes through endothelial cell monolayers: endothelial cells play a key role

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JOURNAL OF ANTIMICROBIAL CHEMOTHERAPY 1999年第4期44卷 465-469页

作者： Hofbauer, R Moser, D Gmeiner, B Kaye, AD Kapiotis, S Wagner, O Frass, M Univ Vienna Dept Med & Chem Lab Diagnost A-1090 Vienna Austria Univ Vienna Dept Maxillofacial Surg A-1090 Vienna Austria Univ Vienna Inst Med Chem A-1090 Vienna Austria Univ Vienna Dept Internal Med 1 A-1090 Vienna Austria Texas Tech Univ Hlth Sci Ctr Dept Anaesthesiol & Intens Care Med Lubbock TX 79430 USA

Postoperative inflammation is still viewed as an unresolved problem. During inflammation, leucocytes play a tremendous role and migrate from intravascular spaces into the tissue to attack microorganisms. Different agents, e.g. anaesthetic drugs, are able to influence leucocyte recruitment. Previous studies have investigated the influence of amoxycillin on chemotaxis of leucocytes alone. The aim of our study was to examine the effect of amoxycillin/clavulanic acid (co-amoxiclav) on leucocyte migration through endothelial cell monolayers (ECMs). Human umbilical endothelial cells were cultured on microporous membranes, achieving a monolayer. Polymorphonuclear neutrophil leucocytes (PMNLs) were used in a migration assay. The numbers of untreated PMNLs migrating through untreated ECMs were used as control and set as 100%. PMNLs and/or ECMs were pretreated with co-amoxiclav using clinically relevant as well as higher and lower concentrations. Co-amoxiclav was able to increase PMNL migration through ECMs significantly (P < 0.05) when both cell types were treated (291 +/- 18.7%). When PMNLs or ECMs were treated alone, it could be shown that ECMs were more affected than PMNLs. The greatest effect was shown when both cell types, PMNLs and ECMs, were treated. in conclusion, co-amoxiclav was identified as a potent drug to increase leucocyte transmigration through ECMs. ECMs were also critically involved. Co-amoxiclav also affects endothelial cells.

关键词：阿莫西林棒酸钾合剂/血液阿莫西林棒酸钾合剂/药理学细胞运动/药物作用细胞培养的剂量效应关系药物药物疗法联合/药理学内皮血管/细胞学内皮血管/药物作用内皮血管/生理学中性白细胞/药物作用中性白细胞/生理学女(雌)性人类男(雄)性

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Angiopoietin-1 and angiopoietin-2 activate trophoblast Tie-2 to promote growth and migration during placental development

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AMERICAN JOURNAL OF PATHOLOGY 2000年第6期156卷 2185-2199页

作者： Dunk, C Shams, M Nijjar, S Rhaman, M Qiu, Y Bussolati, B Ahmed, A Univ Birmingham Womens Hosp Dept Reprod & Vasc Biol Div Reprod & Child Hlth Birmingham B15 2TG W Midlands England

Human placental development involves coordinated angiogenesis and trophoblast outgrowth that are compromised in intrauterine growth restriction (IUGR). As Tie-2((-/-)) mice exhibit growth retardation and vascular network malformation, the expression of Tie-2 and its ligands, angiopoietin-1 (Ang-l) and angiopoietin-2 (Ang-a), were investigated in human placenta from normal pregnancies and those complicated by severe NGR, Ribonucleotide protection assays showed no significant change in the expression of Ang-2 mRNA between gestationally matched normal and IUGR placentas;however, immunoblots revealed that Ang-2 protein was significantly decreased in IUGR, suggesting that this may contribute to the abnormal development of the villous vasculature, In situ hybridization studies showed that Ang-l and Tie-2 were detected in the cyto/syncytiotrophoblast bilayer in first-trimester placenta, whereas Ang-2 mRNA was restricted to the cytotrophoblast, suggesting their role in trophoblast function. At term, Ang-l mRNA and immunoreactive protein were restricted to the paravascular tissues of the primary stem villi, supporting its role in vessel maturation. In contrast, Ang-2 was expressed throughout the term villous core, perhaps to permit the developing placental vascular network to remain in a state of fluidity, As these studies also revealed that trophoblast, in addition to endothelial cells, expressed Tie-2 receptors,we Investigated the potential role of Ang-1/Ang-2 on trophoblast proliferation, migration, and the release of NO. Using spontaneously transformed first-trimester trophoblast cell lines that exhibit cytotrophoblast-like (ED27) and extravillous trophoblast-like (ED77) properties, we show that the addition of Ang-2 (250 ng/ml) stimulated DNA synthesis in ED27 trophoblast cells and triggered the release of NO. Ang-l stimulated trophoblast (ED77) migration in a dose-dependent manner that was inhibited by recombinant Tie-2-FC, These data thus imply, for the first time, a

关键词：血管生成素1 血管生成素2 细胞分裂/药物作用细胞运动/药物作用胎儿生长迟缓/代谢免疫学技术原位杂交膜糖蛋白类/遗传学膜糖蛋白类/药理学肿瘤蛋白质类/生理学一氧化氮/代谢胎盘/代谢胎盘/生理学蛋白质类/遗传学蛋白质类/药理学原癌基因蛋白质类 RNA 信使/代谢受体 TIE-2 参考值逆转录聚合酶链反应组织分布滋养层/细胞学滋养层/药物作用滋养层/代谢女(雌)性人类妊娠

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Position-dependent linkages of fibronectin-integrin-cytoskeleton

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PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2000年第2期97卷 692-697页

作者： Nishizaka, T Shi, Q Sheetz, MP Duke Univ Med Ctr Dept Cell Biol Durham NC 27710 USA Waseda Univ Sch Sci & Engn Dept Phys Shinjuku Ku Tokyo 1698555 Japan

Position-dependent cycling of integrin interactions with both the cytoskeleton and extracellular matrix (ECM) is essential for cell spreading, migration, and wound healing. Whether there are regional changes in integrin concentration, ligand affinity or cytoskeleton crosslinking of liganded integrins has been unclear. Here, we directly demonstrate a position-dependent binding and release cycle of fibronectin-integrin-cytoskeleton interactions with preferential binding at the front of motile 3T3 fibroblasts and release at the endoplasm-ectoplasm boundary. Polystyrene beads coated with low concentrations of an integrin-binding fragment of fibronectin (fibronectin type III domains 7-10) were 3-4 times more likely to bind to integrins when placed within 0.5 microns vs, 0.5-3 microns from the leading edge. Integrins were not concentrated at the leading edge, nor did anti-integrin antibody-coated beads bind preferentially at the leading edge. However, diffusing liganded integrins attached to the cytoskeleton preferentially at the leading edge, Cytochalasin inhibited edge binding, which suggested that cytoskeleton binding to the integrins could alter the avidity for ligand beads. Further, at the ectoplasm-endoplasm boundary, the velocity of bead movement decreased, diffusive motion increased, and approximately one-third of the beads were released into the medium. We suggest that cytoskeleton linkage of liganded integrins stabilizes integrin-ECM bonds at the front whereas release of cytoskeleton-integrin links weakens integrin-ECM bonds at the back of lamellipodia.

关键词： 3T3细胞/细胞学 3T3细胞/代谢细胞膜/代谢细胞运动/药物作用细胞松弛素B/药理学细胞骨架/代谢纤连蛋白类/代谢整合素类/代谢微球体蛋白质结合/药物作用动物小鼠

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Role of inducible nitric oxide synthase in leukocyte extravasation in vivo

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第3期257卷 684-686页

作者： Cockrell, A Laroux, FS Jourd'heuil, D Kawachi, S Gray, L Van der Heyde, H Grisham, MB Louisiana State Univ Med Ctr Dept Mol & Cellular Physiol Shreveport LA 71130 USA Louisiana State Univ Med Ctr Dept Microbiol & Immunol Shreveport LA 71130 USA

Several recent studies have suggested that nitric oxide (NO) derived from the inducible isoform of NO synthase (NOS) may act as an endogenous modulator of the inflammatory response by inhibiting adhesion of leukocytes to endothelial cells in vitro. Few studies have addressed specifically the role of iNOS in regulating leukocyte recruitment in vivo in a model of acute inflammation. Thus, the objective of this study was to assess the role of iNOS in modulating neutrophil (PMN) extravasation in an oyster glycogen-induced model of acute peritonitis in rats. Data obtained in the present study demonstrates that injection (IP) of oyster glycogen induces massive and selective PMN recruitment into the peritoneal cavity of rats at 6 hrs following OG administration. These extravasated cells were found to contain significant amounts of iNOS protein as assessed by Western blot analysis. Treatment of rats with the selective iNOS inhibitor L-iminoethyl-lysine (L-NIL) dramatically reduced NO levels in lavage fluid as measured by de. creases in nitrate and nitrite concentrations without significantly affecting iNOS protein levels. Although L-NIL inhibited NO production by >70%, it did not alter oyster glycogen-induced PMN recruitment when compared to vehicle-treated rats. We conclude that PMN-associated, iNOS-derived NO does not play an important role in modulating extravasation of these leukocytes in this model of acute inflammation. (C) 1999 Academic Press.

关键词：急性病腹水液/代谢印迹法蛋白质细胞运动/药物作用疾病模型动物酶诱导/药物作用糖原/投药和剂量糖原/药理学炎症/化学诱导炎症/酶学炎症/代谢炎症/病理学赖氨酸/类似物和衍生物赖氨酸/药理学中性白细胞/细胞学中性白细胞/药物作用中性白细胞/免疫学中性白细胞/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/代谢牡蛎科腹膜炎/化学诱导腹膜炎/酶学腹膜炎/代谢腹膜炎/病理学大鼠近交Lew 动物女(雌)性大鼠

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CCL chemokines and asthma

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IMMUNOLOGY TODAY 2000年第5期21卷 235-242页

作者： Teran, LM Inst Nacl Enfermedades Resp Mexico City DF Mexico

Airway eosinophilia is a characteristic of bronchial asthma. Eosinophils are considered to cause tissue damage through the release of toxic proteases, lipid mediators, cytokines and oxygen free radicals. The discovery of chemokines and the demonstration that some members of this cytokine superfamily are implicated in the recruitment of eosinophils offers an opportunity for a novel therapeutic approach in asthma.

关键词：哮喘/免疫学哮喘/病毒学细胞运动/药物作用趋化因子 CC 趋化因子嗜酸细胞/免疫学细胞因子类/化学细胞因子类/代谢细胞因子类/药理学嗜酸细胞/药物作用嗜酸细胞/免疫学上皮细胞/代谢配体单核细胞化学吸引蛋白质类/免疫学单核细胞化学吸引蛋白质类/药理学受体趋化因子/代谢呼吸道黏膜/细胞学呼吸道黏膜/免疫学人类

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Stimulation of cell invasion and migration by alcohol in breast cancer cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 2000年第2期273卷 448-453页

作者： Meng, QH Gao, B Goldberg, ID Rosen, EM Fan, SJ Long Isl Jewish Med Ctr Dept Radiat Oncol Oncol Mol Lab New Hyde Pk NY 11042 USA Virginia Commonwealth Univ Coll Med Dept Pharmacol & Toxicol Richmond VA 23284 USA

Increasing epidemiological studies suggest that alcohol consumption confers a high risk for development of breast cancer. In this study, we found that biologically relevant concentrations of alcohol elicited a significant stimulation of cell adhesion, migration, and invasion in MCF-7 human breast cancer cells. Moreover, the promotion of invasion and migration potential by alcohol was associated with the significant decrease of E-cadherin, alpha, beta, and gamma three major catenin, and BRCA1 expression. In addition, an enhanced expression of BRCA1 significantly blocked alcohol-stimulated cell invasion. Thus, our present study suggests that alcohol as a breast cancer risk factor plays an important role not only in carcinogenesis, but also in promotion of cell invasion and migration. (C) 2000 Academic Press.

关键词：饮酒乳腺肿瘤/病因学乳腺肿瘤/遗传学乳腺肿瘤/病理学钙黏着糖蛋白类/遗传学细胞黏附/药物作用细胞运动/药物作用细胞支架蛋白质类/遗传学乙醇/毒性基因表达基因 BRCA1 肿瘤侵润 RNA 信使/遗传学 RNA 信使/代谢 RNA 肿瘤/遗传学 RNA 肿瘤/代谢危险因素肿瘤细胞培养的女(雌)性人类

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DIMETHYL-SULFOXIDE - TOOL IN STUDY OF SPERM MOTILITY CONTROL

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ANNALS OF THE NEW YORK ACADEMY OF SCIENCES 1975年第JAN27期243卷 297-305页

作者： NELSON, L MED COLL OHIO DEPT PHYSIOL TOLEDO OH 43614 USA

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Receptor-mediated inhibition of keratinocyte migration by nicotine involves modulations of calcium influx and intracellular concentration

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 2000年第3期293卷 973-981页

作者： Zia, SH Ndoye, A Lee, TX Webber, RJ Grando, SA Univ Calif Davis Med Ctr Dept Dermatol Sacramento CA 95817 USA Univ Minnesota Dept Dermatol Minneapolis MN 55455 USA Res & Diagnost Antibodies Richmond CA USA

Early stages of wound healing rely on the ability of keratinocytes (KCs) to move over the denuded dermis to re-epithelialize the defect. The agarose gel keratinocyte outgrowth system (AGKOS) is an in vitro model of skin re-epithelialization designed to study the migratory function of KCs. Endogenously secreted acetylcholine controls crawling locomotion of KCs in AGKOS by binding to the cholinergic receptors of both the nicotinic and the muscarinic classes that are expressed by KCs. In this study, we used AGKOS to elucidate the nicotinic pathway of cholinergic control of keratinocyte migration. Activation of the nicotinic acetylcholine receptors decreased the migration distance of KC in a dose-dependent fashion without altering cell viability. Nicotine also increased in a dose-dependent manner transmembrane influx of Ca-45(2+) and caused a transient rise in the concentration of [Ca2+](i). Perfect correlation between concentration responses found in the migration and Ca-45(2+) influx assays suggested that nicotine-induced inhibition of crawling locomotion relies on modulation of Ca2+ metabolism in KCs. The effects of nicotine could be mediated by the alpha 3- and the alpha 7-containing nicotinic receptors visualized on KCs by immunostaining. Long-term incubation with nicotine upregulated alpha 7 and down-regulated alpha 3 expression. Thus, nicotine exerts inhibitory effects on keratinocyte migration, and Ca2+ serves as a second messenger in the signaling pathway. These results help explain deleterious effects of nicotine on wound re-epithelialization, and suggest that smoking may delay wound healing via nicotinic receptor-mediated pathway.

关键词：钙/代谢细胞运动/药物作用细胞培养的角蛋白细胞/化学角蛋白细胞/生理学尼古丁/药理学受体烟碱/分析受体烟碱/生理学伤口愈合动物人类兔

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Inhibitory effect of omeprazole on transmigration of leukocytes through endothelial cell monolayers and leukocyte adhesion

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MICROVASCULAR RESEARCH 2000年第1期59卷 169-171页

作者： Hofbauer, R Losert, H Gmeiner, B Wagner, O Kapiotis, S Frass, M Kaye, AD Univ Vienna Dept Med A-1090 Vienna Austria Univ Vienna Chem Lab Diagnost A-1090 Vienna Austria Univ Vienna MICU Dept Internal Med 1 A-1090 Vienna Austria Univ Vienna Inst Med Chem A-1090 Vienna Austria Texas Tech Univ Hlth Sci Ctr Dept Anesthesiol Lubbock TX 79430 USA

During inflammation, polymorphonuclear neutro-phil leukocytes (PMNL) play a tremendous role. They migrate rapidl / from the vascular space into ths tissue to destroy invading microorganisms (Carlos and Har-lan, 1994). The influence of nonsteroidal anti-inflammatory drugs, e.g., ibuprofen, or of low-molecular-weight heparin on leukocyte function is well investigated using an I'M vitro double-chamber migration assay including endothelial cell monolayers (ECM; Hofbauer ct al, 1998,1999).

关键词：细胞黏附/药物作用细胞运动/药物作用细胞培养的共同培养技术剂量效应关系药物内皮血管/细胞学白细胞黏连抑制试验白细胞/细胞学白细胞/药物作用奥美拉唑/药理学人类

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The kinase inhibitor fasudil (HA-1077) reduces intimal hyperplasia through inhibiting migration and enhancing cell loss of vascular smooth muscle cells

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BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 1999年第1期262卷 211-215页

作者： Negoro, N Hoshiga, M Seto, M Kohbayashi, E Ii, M Fukui, R Shibata, N Nakakoji, T Nishiguchi, F Sasaki, Y Ishihara, T Ohsawa, N Osaka Med Coll Dept Internal Med 1 Takatsuki Osaka 5698686 Japan Asahi Chem Ind Co Ltd Life Sci Res Ctr Frontier 21 Project Shizuoka 4160934 Japan

Smooth muscle cell (SMC) migration plays an important role in restenosis after angioplasty, Myosin phosphorylation is necessary for cell migration. Fasudil is an inhibitor of protein kinases, including myosin light chain kinase and Rho associated kinase, thereby inhibiting myosin phosphorylation, and it has been clinically used to prevent vasospasm following subarachnoid hemorrage, Based on these findings, we examined the antimigrative action of fasudil. In SMC (SM-3), fasudil (1-100 mu M) inhibited SMC migration in a dose-dependent man ner (p < 0,001), Fasudil suppressed actin stress fiber formation dose dependently. In rabbit carotid artery, fasudil (10 mg/kg/day) markedly reduced intimal hyperplasia 14 days following balloon injury. Cell kinetic study showed that fasudil did not affect proliferation but enhanced cell loss in the media after injury. We concluded that fasudil reduced neointimal formation after balloon injury through both inhibiting migration and enhancing cell loss of medial SMC. (C) 1999 Academic Press.

关键词：肌动蛋白类/代谢主动脉气囊扩张术颈动脉损伤细胞计数/药物作用细胞分裂/药物作用细胞运动/药物作用细胞培养的剂量效应关系药物增生/病理学微丝/药物作用微丝/代谢肌平滑血管/细胞学肌平滑血管/药物作用肌平滑血管/损伤肌平滑血管/病理学蛋白激酶抑制剂时间因素血管内膜/药物作用血管内膜/损伤血管内膜/病理学伤口愈合/药物作用动物人类男(雄)性兔

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