BibSonomyburst/user/kanefendt/physiologyBibSonomy RSS feed for /user/kanefendt/physiology2012-02-16T17:07:34+01:00http://www.bibsonomy.org/bibtex/2fe9b6da17080b89b77fd623f65128cf0/kanefendtkanefendt2010-02-05T11:28:39+01:00&amp; Adhesion Albuminuria Angiotensin Animals Atherosclerosis B Blood C57BL Cardiovascular Cell Cells Chain Chloride Cultured Dietary Diseases Endothelial Ester Expression Factor-alpha Fusion Gene Humans Hypertension I-kappa II III Inbred Inflammation Intercellular Kidney Methyl Mice Models Molecule-1 NF-kappa NG-Nitroarginine Necrosis Nephritis Nitric Organ Oxide Polymerase Pressure Proteins Reaction Receptor Recombinant Regulation Research Reverse Signal Sodium Specificity Synthase TIE-1 Transcriptase Transduction Transgenic Tumor Type Vascular antagonists biosynthesis blood cells complications control etiology genetics inhibitors metabolism physiology physiopathology prevention protein toxicity <span class="authorEditorList"><a href="/author/Henke">N. Henke</a>, <a href="/author/Schmidt-Ullrich">R. Schmidt-Ullrich</a>, <a href="/author/Dechend">R. Dechend</a>, <a href="/author/Park">J. K. Park</a>, <a href="/author/Qadri">F. Qadri</a>, <a href="/author/Wellner">M. Wellner</a>, <a href="/author/Obst">M. Obst</a>, <a href="/author/Gross">V. Gross</a>, <a href="/author/Dietz">R. Dietz</a>, <a href="/author/Luft">F. C. Luft</a>, <a href="/author/Scheidereit">C. Scheidereit</a>, and <a href="/author/Muller">D. N. Muller</a> </span><em>Circ.Res.</em> <em>101(3):268-276</em> (<em>2007</em>)Fri Feb 05 11:28:39 CET 2010Circ.Res.3268-276Vascular endothelial cell-specific NF-kappaB suppression attenuates hypertension-induced renal damage1012007& Adhesion Albuminuria Angiotensin Animals Atherosclerosis B Blood C57BL Cardiovascular Cell Cells Chain Chloride Cultured Dietary Diseases Endothelial Ester Expression Factor-alpha Fusion Gene Humans Hypertension I-kappa II III Inbred Inflammation Intercellular Kidney Methyl Mice Models Molecule-1 NF-kappa NG-Nitroarginine Necrosis Nephritis Nitric Organ Oxide Polymerase Pressure Proteins Reaction Receptor Recombinant Regulation Research Reverse Signal Sodium Specificity Synthase TIE-1 Transcriptase Transduction Transgenic Tumor Type Vascular antagonists biosynthesis blood cells complications control etiology genetics inhibitors metabolism physiology physiopathology prevention protein toxicity Nuclear factor kappa B (NF-kappaB) participates in hypertension-induced vascular and target-organ damage. We tested whether or not endothelial cell-specific NF-kappaB suppression would be ameliorative. We generated Cre/lox transgenic mice with endothelial cell-restricted NF-kappaB super-repressor IkappaBalphaDeltaN (Tie-1-DeltaN mice) overexpression. We confirmed cell-specific IkappaBalphaDeltaN expression and reduced NF-kappaB activity after TNF-alpha stimulation in primary endothelial cell culture. To induce hypertension with target-organ damage, we fed mice a high-salt diet and N(omega)-nitro-l-arginine-methyl-ester (L-NAME) and infused angiotensin (Ang) II. This treatment caused a 40-mm Hg blood pressure increase in both Tie-1-DeltaN and control mice. In contrast to control mice, Tie-1-DeltaN mice developed a milder renal injury, reduced inflammation, and less albuminuria. RT-PCR showed significantly reduced expression of the NF-kappaB targets VCAM-1 and ICAM-1, compared with contrhttp://www.bibsonomy.org/bibtex/2909639ca243007f0137115714f190d36/kanefendtkanefendt2010-02-05T11:28:39+01:00A Angiopoietins Animals Biological Cells Cultured Endothelial Factor Growth Human Humans Inflammation Lymphangiogenesis Lymphatic Lymphedema Models Proteins Receptors Research Substances TIE Transport Vascular Vesicular Vessels analysis cells cytology physiology protein <span class="authorEditorList"><a href="/author/Makinen">T. Makinen</a>, <a href="/author/Norrmen">C. Norrmen</a>, and <a href="/author/Petrova">T. V. Petrova</a> </span><em>Cell Mol.Life Sci.</em> <em>64(15):1915-1929</em> (<em>2007</em>)Fri Feb 05 11:28:39 CET 2010Cell Mol.Life Sci.151915-1929Molecular mechanisms of lymphatic vascular development642007A Angiopoietins Animals Biological Cells Cultured Endothelial Factor Growth Human Humans Inflammation Lymphangiogenesis Lymphatic Lymphedema Models Proteins Receptors Research Substances TIE Transport Vascular Vesicular Vessels analysis cells cytology physiology protein Lymphatic vasculature has recently emerged as a prominent area in biomedical research because of its essential role in the maintenance of normal fluid homeostasis and the involvement in pathogenesis of several human diseases, such as solid tumor metastasis, inflammation and lymphedema. Identification of lymphatic endothelial specific markers and regulators, such as VEGFR-3, VEGF-C/D, PROX1, podoplanin, LYVE-1, ephrinB2 and FOXC2, and the development of mouse models have laid a foundation for our understanding of the major steps controlling growth and remodeling of lymphatic vessels. In this review we summarize recent advances in the field and discuss how this knowledge as well as use of model organisms, such as zebrafish and Xenopus, should allow further in depth analysis of the lymphatic vascular systemhttp://www.bibsonomy.org/bibtex/286090cbc034bdaa48e8da2ccda1fc004/kanefendtkanefendt2010-02-05T11:28:39+01:00Antibodies Biological Epidermal Expression Factor Gene Growth Human Humans Immunohistochemistry Markers Monoclonal Neoplasms Neoplastic Prognosis Receptor Regulation Tyrosine analysis drug effects etiology identify pathology physiology response therapeutic therapy use <span class="authorEditorList"><a href="/author/Tos">A. P. Dei Tos</a> </span><em>Int.J.Biol.Markers</em> <em>22(1 Suppl 4):S3-S9</em> (<em>2007</em>)Fri Feb 05 11:28:39 CET 2010Int.J.Biol.Markers1 Suppl 4S3-S9The biology of epidermal growth factor receptor and its value as a prognostic/predictive factor222007Antibodies Biological Epidermal Expression Factor Gene Growth Human Humans Immunohistochemistry Markers Monoclonal Neoplasms Neoplastic Prognosis Receptor Regulation Tyrosine analysis drug effects etiology identify pathology physiology response therapeutic therapy use Receptor tyrosine kinases play a major role in human carcinogenesis. Overexpression of the epidermal growth factor receptor (EGFR) has been associated with poor clinical outcome in several types of cancer. In principle, as with HER2, the EGFR status of a tumor should predict the likelihood of response to EGFR-targeted therapy. However, clinical data have failed to demonstrate a relationship between EGFR expression and response to the EGFR-targeted compounds cetuximab, gefitinib and erlotinib. Recently, patients reported to be EGFR negative have been shown to respond to cetuximab. Possible explanations include methodological failures or most likely heterogeneity and complexity of the mechanisms of EGFR-mediated molecular carcinogenesis. Immunohistochemistry is the most widely used method for measuring EGFR expression; however, its value is limited by lack of methodological standardization. Other approaches to measuring EGFR such as amplification assays are currently being introduced buthttp://www.bibsonomy.org/bibtex/224ae23315709946658083795ddc2c4f5/kanefendtkanefendt2010-02-05T11:28:39+01:00Agents Angiogenesis Animals Antineoplastic Blood Endothelium Humans Inhibitors Neoplasms Neovascularization Pathologic Physiologic Platelets RANGE Research drug effects genetics pathology pharmacology physiology therapeutic therapy use <span class="authorEditorList"><a href="/author/Folkman">J. Folkman</a> </span><em>Nat.Rev.Drug Discov.</em> <em>6(4):273-286</em> (<em>2007</em>)Fri Feb 05 11:28:39 CET 2010Nat.Rev.Drug Discov.4273-286Angiogenesis: an organizing principle for drug discovery?62007Agents Angiogenesis Animals Antineoplastic Blood Endothelium Humans Inhibitors Neoplasms Neovascularization Pathologic Physiologic Platelets RANGE Research drug effects genetics pathology pharmacology physiology therapeutic therapy use Angiogenesis--the process of new blood-vessel growth--has an essential role in development, reproduction and repair. However, pathological angiogenesis occurs not only in tumour formation, but also in a range of non-neoplastic diseases that could be classed together as 'angiogenesis-dependent diseases'. By viewing the process of angiogenesis as an 'organizing principle' in biology, intriguing insights into the molecular mechanisms of seemingly unrelated phenomena might be gained. This has important consequences for the clinical use of angiogenesis inhibitors and for drug discovery, not only for optimizing the treatment of cancer, but possibly also for developing therapeutic approaches for various diseases that are otherwise unrelated to each otherhttp://www.bibsonomy.org/bibtex/2602435fc1730c5168f565863b795701d/kanefendtkanefendt2010-02-05T11:28:39+01:00&amp; Adaptor Antibodies Benzenesulfonates Biological Delivery Diseases Drug Enzyme Heart Human Humans Indoles Inhibitors Kinase Kinases Models Monoclonal Mutation Neoplasms Protein Protein-Tyrosine Proteins Proto-Oncogene Pyridines Pyrroles Quinazolines Research Signal Systems Transducing Tyrosine adverse antagonists c-abl cells chemically development drug effects growth induced inhibitors physiology protein response therapy toxicity <span class="authorEditorList"><a href="/author/Force">T. Force</a>, <a href="/author/Krause">D. S. Krause</a>, and <a href="/author/van Etten">R. A. van Etten</a> </span><em>Nat.Rev.Cancer</em> <em>7(5):332-344</em> (<em>2007</em>)Fri Feb 05 11:28:39 CET 2010Nat.Rev.Cancer5332-344Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition72007& Adaptor Antibodies Benzenesulfonates Biological Delivery Diseases Drug Enzyme Heart Human Humans Indoles Inhibitors Kinase Kinases Models Monoclonal Mutation Neoplasms Protein Protein-Tyrosine Proteins Proto-Oncogene Pyridines Pyrroles Quinazolines Research Signal Systems Transducing Tyrosine adverse antagonists c-abl cells chemically development drug effects growth induced inhibitors physiology protein response therapy toxicity Cancer therapy has progressed remarkably in recent years. In no area has this been more apparent than in the development of "targeted therapies", particularly those using drugs that inhibit the activity of certain tyrosine kinases, activating mutations or amplifications of which are causal, or strongly contributory, to tumorigenesis. However, some of these therapies have been associated with toxicity to the heart. Here we summarize what is known about the cardiotoxicity of cancer drugs that target tyrosine kinases. We focus on basic mechanisms through which interruption of specific signalling pathways leads to cardiomyocyte dysfunction and/or death, and contrast this with therapeutic responses in cancer cellshttp://www.bibsonomy.org/bibtex/2d4a90a7d323e3fd99974bd06b89854d3/kanefendtkanefendt2010-02-05T11:28:39+01:0080 A Adult Age Aged Antigen Biological Case-Control Distribution Endothelial Factor Growth Humans Immunoassay Male Markers Middle Neoplasm Neoplasms Nonparametric Organ Population Prognosis Prostate Prostate-Specific Prostatic Retrospective Size Staging Statistics Studies Tumor Vascular and blood methods over pathology physiology <span class="authorEditorList"><a href="/author/Duque">J. L. Duque</a>, <a href="/author/Loughlin">K. R. Loughlin</a>, <a href="/author/Adam">R. M. Adam</a>, <a href="/author/Kantoff">P. Kantoff</a>, <a href="/author/Mazzucchi">E. Mazzucchi</a>, and <a href="/author/Freeman">M. R. Freeman</a> </span><em>Clinics.</em> <em>61(5):401-408</em> (<em>2006</em>)Fri Feb 05 11:28:39 CET 2010Clinics.5401-408Measurement of plasma levels of vascular endothelial growth factor in prostate cancer patients: relationship with clinical stage, Gleason score, prostate volume, and serum prostate-specific antigen61200680 A Adult Age Aged Antigen Biological Case-Control Distribution Endothelial Factor Growth Humans Immunoassay Male Markers Middle Neoplasm Neoplasms Nonparametric Organ Population Prognosis Prostate Prostate-Specific Prostatic Retrospective Size Staging Statistics Studies Tumor Vascular and blood methods over pathology physiology PURPOSE: This study focused on circulating levels of vascular endothelial growth factor in patients with prostate cancer compared to a normal population. METHODS: We analyzed 26 normal individuals and 80 patients with prostate cancer. Blood was drawn from all subjects, and plasma was extracted to determine the concentration of vascular endothelial growth factor using a quantitative immunoassay technique (ELISA-enzyme-linked immunosorbent assay). RESULTS: The median plasma level of vascular endothelial growth factor was significantly elevated in patients with metastatic disease compared to patients with localized disease and with healthy controls. Patients with serum prostate-specific antigen > 20 ng/mL had significantly higher levels of plasma vascular endothelial growth factor than patients with serum prostate-specific antigen < 20 ng/mL. There was a trend for patients with a Gleason score of 8 to 10 to have higher levels of plasma vascular endothelial growth factor when compared to phttp://www.bibsonomy.org/bibtex/28e3bb24f0d5fe444f2147966afdd05fb/kanefendtkanefendt2010-02-05T11:28:39+01:00Aging Animals Cell Cells Development Division Embryonic Endothelial Endothelium Factor Growth Human Humans Japan Ligands Lymphangiogenesis Lymphatic Lymphedema Neovascularization Pathologic Physiologic Placenta Receptor-1 Receptor-2 Research Signal System Transduction Tyrosine Vascular Vertebrates cells cytology genetics physiology physiopathology response <span class="authorEditorList"><a href="/author/Shibuya">M. Shibuya</a>, and <a href="/author/Claesson-Welsh">L. Claesson-Welsh</a> </span><em>Exp.Cell Res.</em> <em>312(5):549-560</em> (<em>2006</em>)Fri Feb 05 11:28:39 CET 2010Exp.Cell Res.5549-560Signal transduction by VEGF receptors in regulation of angiogenesis and lymphangiogenesis3122006Aging Animals Cell Cells Development Division Embryonic Endothelial Endothelium Factor Growth Human Humans Japan Ligands Lymphangiogenesis Lymphatic Lymphedema Neovascularization Pathologic Physiologic Placenta Receptor-1 Receptor-2 Research Signal System Transduction Tyrosine Vascular Vertebrates cells cytology genetics physiology physiopathology response The VEGF/VPF (vascular endothelial growth factor/vascular permeability factor) ligands and receptors are crucial regulators of vasculogenesis, angiogenesis, lymphangiogenesis and vascular permeability in vertebrates. VEGF-A, the prototype VEGF ligand, binds and activates two tyrosine kinase receptors: VEGFR1 (Flt-1) and VEGFR2 (KDR/Flk-1). VEGFR1, which occurs in transmembrane and soluble forms, negatively regulates vasculogenesis and angiogenesis during early embryogenesis, but it also acts as a positive regulator of angiogenesis and inflammatory responses, playing a role in several human diseases such as rheumatoid arthritis and cancer. The soluble VEGFR1 is overexpressed in placenta in preeclampsia patients. VEGFR2 has critical functions in physiological and pathological angiogenesis through distinct signal transduction pathways regulating proliferation and migration of endothelial cells. VEGFR3, a receptor for the lymphatic growth factors VEGF-C and VEGF-D, but not for VEGF-A, reguhttp://www.bibsonomy.org/bibtex/2c24011977ff0738124791c547dd0d0d9/kanefendtkanefendt2010-02-05T11:28:39+01:00&amp; Adaptation Animals Cardiac Cardiomegaly Cell Contraction Differentiation Diseases Failure Growth Heart Humans Hypertension Myocardial Myocytes Neovascularization Physiologic Physiological Proteins Proto-Oncogene Signal Sports Transduction c-akt cytology development embryology genetics growth metabolism pathology physiology physiopathology protein <span class="authorEditorList"><a href="/author/Shiojima">I. Shiojima</a>, and <a href="/author/Walsh">K. Walsh</a> </span><em>Genes Dev.</em> <em>20(24):3347-3365</em> (<em>2006</em>)Fri Feb 05 11:28:39 CET 2010Genes Dev.243347-3365Regulation of cardiac growth and coronary angiogenesis by the Akt/PKB signaling pathway202006& Adaptation Animals Cardiac Cardiomegaly Cell Contraction Differentiation Diseases Failure Growth Heart Humans Hypertension Myocardial Myocytes Neovascularization Physiologic Physiological Proteins Proto-Oncogene Signal Sports Transduction c-akt cytology development embryology genetics growth metabolism pathology physiology physiopathology protein Postnatal growth of the heart is primarily achieved through hypertrophy of individual myocytes. Cardiac growth observed in athletes represents adaptive or physiological hypertrophy, whereas cardiac growth observed in patients with hypertension or valvular heart diseases is called maladaptive or pathological hypertrophy. These two types of hypertrophy are morphologically, functionally, and molecularly distinct from each other. The serine/threonine protein kinase Akt is activated by various extracellular stimuli in a phosphatidylinositol-3 kinase-dependent manner and regulates multiple aspects of cellular functions including survival, growth and metabolism. In this review we will discuss the role of the Akt signaling pathway in the heart, focusing on the regulation of cardiac growth, contractile function, and coronary angiogenesis. How this signaling pathway contributes to the development of physiological/pathological hypertrophy and heart failure will also be discussedhttp://www.bibsonomy.org/bibtex/267ae74502331a25b179814c5fd6bc59c/kanefendtkanefendt2010-02-05T11:28:39+01:00&amp; Agents Angiogenesis Animals Binding Biological Blood Carcinogens Cells Endothelial Genes Humans Inducing Inhibitors Laboratories Ligands Models Neoplasms Neovascularization Notch Pathologic Receptors Signal Suppressor Transduction Tumor Vessels blood cells development growth metabolism physiology supply therapy <span class="authorEditorList"><a href="/author/Rehman">A. O. Rehman</a>, and <a href="/author/Wang">C. Y. Wang</a> </span><em>Trends Cell Biol.</em> <em>16(6):293-300</em> (<em>2006</em>)Fri Feb 05 11:28:39 CET 2010Trends Cell Biol.6293-300Notch signaling in the regulation of tumor angiogenesis162006& Agents Angiogenesis Animals Binding Biological Blood Carcinogens Cells Endothelial Genes Humans Inducing Inhibitors Laboratories Ligands Models Neoplasms Neovascularization Notch Pathologic Receptors Signal Suppressor Transduction Tumor Vessels blood cells development growth metabolism physiology supply therapy The Notch signaling pathway is conserved in vertebrates and invertebrates and is involved in many developmental processes. Notch receptors and ligands are expressed on the cell surface enabling interactions between adjacent cells upon receptor-ligand binding. Notch signaling molecules have an important well-documented role in vascular development, differentiation, proliferation, apoptosis and tumorigenesis. Recently, several groups have identified the importance of Notch signaling in tumor angiogenesis. Notch activity increases specifically in tumor endothelium and in various tumors types and, in some studies, Notch signaling suppresses angiogenic processes. Because the Notch signaling pathway can mediate communication between various cell types in the tumor microenvironment, interactions between tumor cells and endothelial cells might promote angiogenesis, therefore targeting the Notch pathway might provide a novel strategy for anti-angiogenic therapies. Here, we discuss recent insighhttp://www.bibsonomy.org/bibtex/248716170c028a454d03cdde4372bd3f1/kanefendtkanefendt2010-02-05T11:28:39+01:00A Animals Atherosclerosis Cells Chemistry Development Dna Embryonic Endothelial Factor Female Growth Human Humans Inflammation Japan Metastasis Mice Neoplasm Neoplasms Neovascularization Pathologic Physiologic Pre-Eclampsia Pregnancy Proteins Receptor-1 Receptor-2 Research Signal Transduction Tyrosine Vascular Viral blood cells genetics metabolism physiology physiopathology protein response supply therapy <span class="authorEditorList"><a href="/author/Shibuya">M. Shibuya</a> </span><em>J Biochem.Mol.Biol.</em> <em>39(5):469-478</em> (<em>2006</em>)Fri Feb 05 11:28:39 CET 2010J Biochem.Mol.Biol.5469-478Differential roles of vascular endothelial growth factor receptor-1 and receptor-2 in angiogenesis392006A Animals Atherosclerosis Cells Chemistry Development Dna Embryonic Endothelial Factor Female Growth Human Humans Inflammation Japan Metastasis Mice Neoplasm Neoplasms Neovascularization Pathologic Physiologic Pre-Eclampsia Pregnancy Proteins Receptor-1 Receptor-2 Research Signal Transduction Tyrosine Vascular Viral blood cells genetics metabolism physiology physiopathology protein response supply therapy Vascular endothelial growth factor (VEGF)-A, a major regulator for angiogenesis, binds and activates two tyrosine kinase receptors, VEGFR1 (Flt-1) and VEGFR2 (KDR/Flk-1). These receptors regulate physiological as well as pathological angiogenesis. VEGFR2 has strong tyrosine kinase activity, and transduces the major signals for angiogenesis. However, unlike other representative tyrosine kinase receptors which use the Ras pathway, VEGFR2 mostly uses the Phospholipase-Cgamma-Protein kinase-C pathway to activate MAP-kinase and DNA synthesis. VEGFR2 is a direct signal transducer for pathological angiogenesis including cancer and diabetic retinopathy, thus, VEGFR2 itself and the signaling appear to be critical targets for the suppression of these diseases. VEGFR1 plays dual role, a negative role in angiogenesis in the embryo most likely by trapping VEGF-A, and a positive role in adulthood in a tyrosine kinase-dependent manner. VEGFR1 is expressed not only in endothelial cells but also in machttp://www.bibsonomy.org/bibtex/2463d0b247e477cd3460c6d76976388b8/kanefendtkanefendt2010-02-05T11:28:39+01:00&amp; A Administration Agents Angiogenesis Antineoplastic Biological Blood Clinical Coagulation Drug Endothelial Factor Function Growth Humans Hypertension Inhibitors Left Models Neoplasm Platelets Research Resistance Schedule Signal Thrombosis Topic Transduction Trials Vascular Ventricular administration adverse antagonists as chemically dosage drug effects etiology induced inhibitors physiology toxicity <span class="authorEditorList"><a href="/author/Verheul">H. M. Verheul</a>, and <a href="/author/Pinedo">H. M. Pinedo</a> </span><em>Nat.Rev.Cancer</em> <em>7(6):475-485</em> (<em>2007</em>)Fri Feb 05 11:28:39 CET 2010Nat.Rev.Cancer6475-485Possible molecular mechanisms involved in the toxicity of angiogenesis inhibition72007& A Administration Agents Angiogenesis Antineoplastic Biological Blood Clinical Coagulation Drug Endothelial Factor Function Growth Humans Hypertension Inhibitors Left Models Neoplasm Platelets Research Resistance Schedule Signal Thrombosis Topic Transduction Trials Vascular Ventricular administration adverse antagonists as chemically dosage drug effects etiology induced inhibitors physiology toxicity Contrary to initial expectations, angiogenesis inhibitors can cause toxicities in patients with cancer. The toxicity profiles of these inhibitors reflect the disturbance of growth factor signalling pathways that are important for maintaining homeostasis. Experiences with angiogenesis inhibitors in clinical trials indicate that short-term toxicities are mostly manageable. However, these agents will also be given in prolonged treatment strategies, so we need to anticipate possible long-term toxicities. In addition, understanding the molecular mechanisms involved in the toxicity of angiogenesis inhibition should allow more specific and more potent inhibitors to be developedhttp://www.bibsonomy.org/bibtex/2ee1fa6cc385bc0da43b7dc0595066e27/kanefendtkanefendt2010-02-05T11:28:39+01:00&amp; Adult Aged Animals C Data Doxycycline Elephantiasis Endothelial Factor Female Filarial Filaricides Growth Humans Hydrocele Intercellular Lymphatic Lymphedema Male Microfilaria Middle Molecular Outcome Parasitemia Peptides Plasma Proteins Receptor-3 Research Sequence Signaling System Testicular Testis Treatment Vascular Vessels Wolbachia and antagonists blood drug effects immunology inhibitors isolation parasitology pathology physiology protein purification therapeutic therapy ultrasonography use <span class="authorEditorList"><a href="/author/Debrah">A. Y. Debrah</a>, <a href="/author/Mand">S. Mand</a>, <a href="/author/Specht">S. Specht</a>, <a href="/author/Marfo-Debrekyei">Y. Marfo-Debrekyei</a>, <a href="/author/Batsa">L. Batsa</a>, <a href="/author/Pfarr">K. Pfarr</a>, <a href="/author/Larbi">J. Larbi</a>, <a href="/author/Lawson">B. Lawson</a>, <a href="/author/Taylor">M. Taylor</a>, <a href="/author/Adjei">O. Adjei</a>, and <a href="/author/Hoerauf">A. Hoerauf</a> </span><em>PLoS.Pathog.</em> <em>2(9):e92</em> (<em>2006</em>)Fri Feb 05 11:28:39 CET 2010PLoS.Pathog.9e92Doxycycline reduces plasma VEGF-C/sVEGFR-3 and improves pathology in lymphatic filariasis22006& Adult Aged Animals C Data Doxycycline Elephantiasis Endothelial Factor Female Filarial Filaricides Growth Humans Hydrocele Intercellular Lymphatic Lymphedema Male Microfilaria Middle Molecular Outcome Parasitemia Peptides Plasma Proteins Receptor-3 Research Sequence Signaling System Testicular Testis Treatment Vascular Vessels Wolbachia and antagonists blood drug effects immunology inhibitors isolation parasitology pathology physiology protein purification therapeutic therapy ultrasonography use Lymphatic filariasis is a disease of considerable socioeconomic burden in the tropics. Presently used antifilarial drugs are able to strongly reduce transmission and will thus ultimately lower the burden of morbidity associated with the infection, however, a chemotherapeutic principle that directly induces a halt or improvement in the progression of the morbidity in already infected individuals would constitute a major lead. In search of such a more-effective drug to complement the existing ones, in an area endemic for bancroftian filariasis in Ghana, 33 microfilaremic and 18 lymphedema patients took part in a double-blind, placebo-controlled trial of a 6-wk regimen of 200 mg/day doxycycline. Four months after doxycycline treatment, all patients received 150-200 microg/kg ivermectin and 400 mg albendazole. Patients were monitored for Wolbachia and microfilaria loads, antigenemia, filarial dance sign (FDS), dilation of supratesticular lymphatic vessels, and plasma levels of lymphangiogehttp://www.bibsonomy.org/bibtex/27cd562128bbe2ee505432fc38695f843/kanefendtkanefendt2010-02-05T11:28:39+01:00A Binding Biological Biology Capillaries Dimerization Endothelial Factor Growth Human Humans Ligands Lymphatic Models Muscle Plasma Receptor-1 Research Skeletal States Systems Tyrosine United Vascular Vessels metabolism physiology protein therapy ultrastructure <span class="authorEditorList"><a href="/author/Wu">F. T. Wu</a>, <a href="/author/Stefanini">M. O. Stefanini</a>, <a href="/author/Mac">Gabhann F. Mac</a>, and <a href="/author/Popel">A. S. Popel</a> </span><em>PLoS.One.</em> <em>4(4):e5108</em> (<em>2009</em>)Fri Feb 05 11:28:39 CET 2010PLoS.One.4e5108A compartment model of VEGF distribution in humans in the presence of soluble VEGF receptor-1 acting as a ligand trap42009A Binding Biological Biology Capillaries Dimerization Endothelial Factor Growth Human Humans Ligands Lymphatic Models Muscle Plasma Receptor-1 Research Skeletal States Systems Tyrosine United Vascular Vessels metabolism physiology protein therapy ultrastructure Vascular endothelial growth factor (VEGF), through its activation of cell surface receptor tyrosine kinases including VEGFR1 and VEGFR2, is a vital regulator of stimulatory and inhibitory processes that keep angiogenesis--new capillary growth from existing microvasculature--at a dynamic balance in normal physiology. Soluble VEGF receptor-1 (sVEGFR1)--a naturally-occurring truncated version of VEGFR1 lacking the transmembrane and intracellular signaling domains--has been postulated to exert inhibitory effects on angiogenic signaling via two mechanisms: direct sequestration of angiogenic ligands such as VEGF; or dominant-negative heterodimerization with surface VEGFRs. In pre-clinical studies, sVEGFR1 gene and protein therapy have demonstrated efficacy in inhibiting tumor angiogenesis; while in clinical studies, sVEGFR1 has shown utility as a diagnostic or prognostic marker in a widening array of angiogenesis-dependent diseases. Here we developed a novel computational multi-tissue model http://www.bibsonomy.org/bibtex/271956b27a8f21b1b822b52d005ae329f/kanefendtkanefendt2010-02-05T11:28:39+01:00A Adenocarcinoma Adenoviridae Animals BALB Biological Burden C C57BL Cell Cells Cultured Disease Endothelial Experimental Factor Female Genetic Growth HT29 Heterologous Human Humans Inbred Male Mammary Markers Mice Neoplasm Neoplasms Progression Proliferation Prostatic Receptor-2 Research Solubility Transduction Transfection Transgenic Transplantation Tumor Tyrosine Vascular blood cells genetics metabolism methods pathology physiology protein <span class="authorEditorList"><a href="/author/Ebos">J. M. Ebos</a>, <a href="/author/Lee">C. R. Lee</a>, <a href="/author/Bogdanovic">E. Bogdanovic</a>, <a href="/author/Alami">J. Alami</a>, <a href="/author/Van">Slyke P. Van</a>, <a href="/author/Francia">G. Francia</a>, <a href="/author/Xu">P. Xu</a>, <a href="/author/Mutsaers">A. J. Mutsaers</a>, <a href="/author/Dumont">D. J. Dumont</a>, and <a href="/author/Kerbel">R. S. Kerbel</a> </span><em>Cancer Res.</em> <em>68(2):521-529</em> (<em>2008</em>)Fri Feb 05 11:28:39 CET 2010Cancer Res.2521-529Vascular endothelial growth factor-mediated decrease in plasma soluble vascular endothelial growth factor receptor-2 levels as a surrogate biomarker for tumor growth682008A Adenocarcinoma Adenoviridae Animals BALB Biological Burden C C57BL Cell Cells Cultured Disease Endothelial Experimental Factor Female Genetic Growth HT29 Heterologous Human Humans Inbred Male Mammary Markers Mice Neoplasm Neoplasms Progression Proliferation Prostatic Receptor-2 Research Solubility Transduction Transfection Transgenic Transplantation Tumor Tyrosine Vascular blood cells genetics metabolism methods pathology physiology protein Vascular endothelial growth factor (VEGF) is a potent proangiogenic protein that activates VEGF receptor (VEGFR) tyrosine kinases expressed by vascular endothelial cells. We previously showed that one of these receptors, VEGFR-2, has a truncated soluble form (sVEGFR-2) that can be detected in mouse and human plasma. Because activation of VEGFR-2 plays an important role in tumor angiogenesis, clinical interest in monitoring plasma sVEGFR-2 levels in cancer patients has focused on its potential exploitation as a surrogate biomarker for disease progression as well as assessing efficacy/activity of antiangiogenic drugs, particularly those that target VEGF or VEGFR-2. However, no preclinical studies have been done to study sVEGFR-2 during tumor growth or the mechanisms involved in its modulation. Using spontaneously growing tumors and both localized and metastatic human tumor xenografts, we evaluated the relationship between sVEGFR-2 and tumor burden as well as underlying factors governing http://www.bibsonomy.org/bibtex/294c1263be4532fda2056dce70ae83ab4/kanefendtkanefendt2010-02-05T11:28:39+01:001 Adenocarcinoma Autocrine Breast C Carcinoma Cell Colorectal Communication Endothelial Expression Factor Gene Growth Human Humans Hypoxia Hypoxia-Inducible Line Lung Neoplasms Neoplastic Oxygen Receptor-1 Receptor-2 Receptor-3 Regulation Subunit Survival Tumor Up-Regulation Vascular alpha cells genetics metabolism pathology physiology protein <span class="authorEditorList"><a href="/author/Simiantonaki">N. Simiantonaki</a>, <a href="/author/Jayasinghe">C. Jayasinghe</a>, <a href="/author/Michel-Schmidt">R. Michel-Schmidt</a>, <a href="/author/Peters">K. Peters</a>, <a href="/author/Hermanns">M. I. Hermanns</a>, and <a href="/author/Kirkpatrick">C. J. Kirkpatrick</a> </span><em>Int.J.Oncol.</em> <em>32(3):585-592</em> (<em>2008</em>)Fri Feb 05 11:28:39 CET 2010Int.J.Oncol.3585-592Hypoxia-induced epithelial VEGF-C/VEGFR-3 upregulation in carcinoma cell lines3220081 Adenocarcinoma Autocrine Breast C Carcinoma Cell Colorectal Communication Endothelial Expression Factor Gene Growth Human Humans Hypoxia Hypoxia-Inducible Line Lung Neoplasms Neoplastic Oxygen Receptor-1 Receptor-2 Receptor-3 Regulation Subunit Survival Tumor Up-Regulation Vascular alpha cells genetics metabolism pathology physiology protein Adaptation to hypoxia, a universal hallmark of carcinomas, is a critical step for tumor cell survival and growth. One of the principal regulators of hypoxia-responsive pathways is the transcription factor hypoxia-inducible factor-1 alpha (HIF-1 alpha). Currently, it is known that tumoral production of members of the vascular endothelial growth factor (VEGF)-family (VEGFs) may promote tumor growth and progression by acting on carcinoma cells that express the cognate receptors (VEGFRs). However, the influence of hypoxia in the formation of such a tumoral VEGF/VEGFR loop is not completely understood. In the present study we examined the potential existence of a HIF-1 alpha/VEGF/VEGFR autocrine loop on commonly occurring carcinomas. The experiments were performed on five colorectal carcinoma cell lines, one breast (MCF7) and one lung (A549) adenocarcinoma cell line under normoxic and oxygen stress conditions using HIF-1 alpha-EIA, VEGFs-ELISA as well as RT-PCR and immunofluorescence for VEhttp://www.bibsonomy.org/bibtex/234add54e688548f2fe9b773ddc20d004/kanefendtkanefendt2010-02-05T11:28:39+01:00A Angiogenesis Animals Bone Cells Drug Endothelial Factor Growth Human Humans Inhibitors Marrow Neoplasm Neoplasms Neovascularization Notch Pathologic Proteins Proto-Oncogene Receptors Research Resistance Signal Transduction Vascular blood drug physiology physiopathology protein supply therapeutic therapy use <span class="authorEditorList"><a href="/author/Kerbel">R. S. Kerbel</a> </span><em>N.Engl.J.Med.</em> <em>358(19):2039-2049</em> (<em>2008</em>)Fri Feb 05 11:28:39 CET 2010N.Engl.J.Med.192039-2049Tumor angiogenesis3582008A Angiogenesis Animals Bone Cells Drug Endothelial Factor Growth Human Humans Inhibitors Marrow Neoplasm Neoplasms Neovascularization Notch Pathologic Proteins Proto-Oncogene Receptors Research Resistance Signal Transduction Vascular blood drug physiology physiopathology protein supply therapeutic therapy use http://www.bibsonomy.org/bibtex/2a7d6cab082a8228a14e7c5ba0c50d80c/kanefendtkanefendt2010-02-05T11:28:39+01:00A Acid Adult Aged Assay Biological Blood Bone Cells Citrates Collection Edetic Endothelial Enzyme-Linked Factor Factors Female Growth Healing Heparin Humans Immunohistochemistry Immunosorbent Indicators Lymphokines Male Markers Marrow Megakaryocytes Middle Platelets Reagents Reference Research Sensitivity Specificity Specimen Values Vascular Wound and biosynthesis blood cells cytology methods physiology <span class="authorEditorList"><a href="/author/Banks">R. E. Banks</a>, <a href="/author/Forbes">M. A. Forbes</a>, <a href="/author/Kinsey">S. E. Kinsey</a>, <a href="/author/Stanley">A. Stanley</a>, <a href="/author/Ingham">E. Ingham</a>, <a href="/author/Walters">C. Walters</a>, and <a href="/author/Selby">P. J. Selby</a> </span><em>Br.J Cancer</em> <em>77(6):956-964</em> (<em>1998</em>)Fri Feb 05 11:28:39 CET 2010Br.J Cancer6956-964Release of the angiogenic cytokine vascular endothelial growth factor (VEGF) from platelets: significance for VEGF measurements and cancer biology771998A Acid Adult Aged Assay Biological Blood Bone Cells Citrates Collection Edetic Endothelial Enzyme-Linked Factor Factors Female Growth Healing Heparin Humans Immunohistochemistry Immunosorbent Indicators Lymphokines Male Markers Marrow Megakaryocytes Middle Platelets Reagents Reference Research Sensitivity Specificity Specimen Values Vascular Wound and biosynthesis blood cells cytology methods physiology Vascular endothelial growth factor (VEGF) is a potent angiogenic factor with a key role in several pathological processes, including tumour vascularization. Our preliminary observations indicated higher VEGF concentrations in serum samples than in matched plasma samples. We have now demonstrated that this difference is due to the presence of VEGF within platelets and its release upon their activation during coagulation. In eight healthy volunteers, serum VEGF concentrations ranged from 76 to 854 pg ml(-1) and were significantly higher (P < 0.01) than the matched citrated plasma VEGF concentrations, which ranged from < 9 to 42 pg ml(-1). Using platelet-rich plasma, mean (s.d.) platelet VEGF contents of 0.56 (0.36) pg of VEGF 10(-6) platelets were found. Immunocytochemistry demonstrated the cytoplasmic presence of VEGF within megakaryocytes and other cell types within the bone marrow. From examination of the effects of blood sample processing on circulating VEGF concentrations, it is apphttp://www.bibsonomy.org/bibtex/2ced98b07c2443d24d7f22675eeb52e82/kanefendtkanefendt2010-02-05T11:28:39+01:00A Animals Blood Endothelial Factor Factors Growth Humans Kinase Kinases Laboratories Lymphokines Neoplasms Neovascularization Pathologic Physiologic Protein-Tyrosine Receptor Receptors Research Vascular Vessels blood etiology physiology supply <span class="authorEditorList"><a href="/author/Veikkola">T. Veikkola</a>, and <a href="/author/Alitalo">K. Alitalo</a> </span><em>Semin.Cancer Biol.</em> <em>9(3):211-220</em> (<em>1999</em>)Fri Feb 05 11:28:39 CET 2010Semin.Cancer Biol.3211-220VEGFs, receptors and angiogenesis91999A Animals Blood Endothelial Factor Factors Growth Humans Kinase Kinases Laboratories Lymphokines Neoplasms Neovascularization Pathologic Physiologic Protein-Tyrosine Receptor Receptors Research Vascular Vessels blood etiology physiology supply Angiogenesis, the formation of new blood vessels from pre--existing ones, is central for both normal development and homeostasis as well as in certain pathological conditions. The vascular endothelial growth factors (VEGFs) and their receptors are prime regulators of both physiological and pathological angiogenesis. The different VEGFs have overlapping but specific roles in controlling the growth of new blood vessels. The VEGF receptors transduce signals mediating endothelial cell proliferation, migration, organization into functional vessels and remodeling of the vessel network. In recent years, rapid progress has been made in understanding the receptor-ligand interactions that orchestrate the neovascularization processhttp://www.bibsonomy.org/bibtex/2f972ca58089994549fd1cd42b6836c1d/kanefendtkanefendt2010-02-05T11:28:39+01:00Adult Animals Antigens Blood C CD31 Cardiovascular Cell Chemistry Development Embryo Embryonic Endothelial Endothelium Factor Factors Fetal Gene Growth Hematopoiesis Heterozygote Homozygote Hybridization Immunohistochemistry In Kinase Kinases Ligands Lymphatic Mammalian Mice Neovascularization Physiologic Protein-Tyrosine Receptor Receptor-3 Receptors Research Signal Situ Surface System Targeting Transduction Vascular Vessels analysis and blood embryology genetics physiology supply <span class="authorEditorList"><a href="/author/Dumont">D. J. Dumont</a>, <a href="/author/Jussila">L. Jussila</a>, <a href="/author/Taipale">J. Taipale</a>, <a href="/author/Lymboussaki">A. Lymboussaki</a>, <a href="/author/Mustonen">T. Mustonen</a>, <a href="/author/Pajusola">K. Pajusola</a>, <a href="/author/Breitman">M. Breitman</a>, and <a href="/author/Alitalo">K. Alitalo</a> </span><em>Science</em> <em>282(5390):946-949</em> (<em>1998</em>)Fri Feb 05 11:28:39 CET 2010Science5390946-949Cardiovascular failure in mouse embryos deficient in VEGF receptor-32821998Adult Animals Antigens Blood C CD31 Cardiovascular Cell Chemistry Development Embryo Embryonic Endothelial Endothelium Factor Factors Fetal Gene Growth Hematopoiesis Heterozygote Homozygote Hybridization Immunohistochemistry In Kinase Kinases Ligands Lymphatic Mammalian Mice Neovascularization Physiologic Protein-Tyrosine Receptor Receptor-3 Receptors Research Signal Situ Surface System Targeting Transduction Vascular Vessels analysis and blood embryology genetics physiology supply Vascular endothelial growth factor (VEGF) is a key regulator of blood vessel development in embryos and angiogenesis in adult tissues. Unlike VEGF, the related VEGF-C stimulates the growth of lymphatic vessels through its specific lymphatic endothelial receptor VEGFR-3. Here it is shown that targeted inactivation of the gene encoding VEGFR-3 resulted in defective blood vessel development in early mouse embryos. Vasculogenesis and angiogenesis occurred, but large vessels became abnormally organized with defective lumens, leading to fluid accumulation in the pericardial cavity and cardiovascular failure at embryonic day 9.5. Thus, VEGFR-3 has an essential role in the development of the embryonic cardiovascular system before the emergence of the lymphatic vesselshttp://www.bibsonomy.org/bibtex/2e619d006bfc90bced94ddeca2fcb3daa/kanefendtkanefendt2010-02-05T11:28:39+01:00A Calcium Capillaries Cells Cultured Dose-Response Drug Endothelial Endothelium Enzymologic Expression Factor Factors Gene Growth Human Humans Lymphokines Microcirculation Nitric Oxide Regulation Relationship Research Synthase Time Up-Regulation Vascular cells drug effects metabolism pharmacology physiology protein <span class="authorEditorList"><a href="/author/Hood">J. D. Hood</a>, <a href="/author/Meininger">C. J. Meininger</a>, <a href="/author/Ziche">M. Ziche</a>, and <a href="/author/Granger">H. J. Granger</a> </span><em>Am.J.Physiol</em> <em>274(3 Pt 2):H1054-H1058</em> (<em>1998</em>)Fri Feb 05 11:28:39 CET 2010Am.J.Physiol3 Pt 2H1054-H1058VEGF upregulates ecNOS message, protein, and NO production in human endothelial cells2741998A Calcium Capillaries Cells Cultured Dose-Response Drug Endothelial Endothelium Enzymologic Expression Factor Factors Gene Growth Human Humans Lymphokines Microcirculation Nitric Oxide Regulation Relationship Research Synthase Time Up-Regulation Vascular cells drug effects metabolism pharmacology physiology protein Vascular endothelial growth factor (VEGF) is an endothelium-specific secreted protein that potently stimulates vasodilation, microvascular hyperpermeability, and angiogenesis. Nitric oxide (NO) is also reported to modulate vascular tone, permeability, and capillary growth. Therefore, we hypothesized that VEGF might regulate endothelial production of NO. The production of nitrogen oxides by human umbilical vein endothelial cells (HUVECs) was measured after 1, 12, 24, and 48 h of incubation with VEGF. VEGF treatment resulted in both an acute (1 h) and chronic (> 24 h) stimulation of NO production. Furthermore, Western and Northern blotting revealed a VEGF-elicited, dose-dependent increase in the cellular content of endothelial cell nitric oxide synthase (ecNOS) message and protein that may account for the chronic upregulation of NO production elicited by VEGF. Finally, endothelial cells pretreated with VEGF for 24 h and subsequently exposed to A-23187 for 1 h produced NO at approximately