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1. Full Text DNA methyltransferase inhibition induces mouse embryonic stem cell differentiation into endothelial cells
by Banerjee, Saswati and Bacanamwo, Methode
Experimental Cell Research, ISSN 0014-4827, 2010, Volume 316, Issue 2, pp. 172 - 180
Understanding endothelial cell (EC) differentiation is a step forward in tissue engineering, controlling angiogenesis, and endothelial dysfunction. We... 
Embryonic stem cell | DNA methylation | Differentiation | Endothelial cells | VASCULAR DEVELOPMENT | VASCULOGENESIS | VEGF | CARDIOMYOCYTES | MATURATION | HISTONE METHYLATION | CANCER | CELL BIOLOGY | IN-VITRO | HEMATOPOIETIC PROGENITOR CELLS | ONCOLOGY | DISEASE | Embryonic Stem Cells - metabolism | Neovascularization, Physiologic - drug effects | Embryonic Stem Cells - cytology | Cadherins - metabolism | Gene Expression - drug effects | Gene Expression - genetics | Bone Morphogenetic Protein 4 - genetics | von Willebrand Factor - genetics | DNA (Cytosine-5-)-Methyltransferases - antagonists & inhibitors | Vascular Endothelial Growth Factor A - genetics | Antigens, CD - genetics | Promoter Regions, Genetic - genetics | Antigens, CD - metabolism | Octamer Transcription Factor-3 - genetics | Receptor, TIE-2 - metabolism | Cadherins - genetics | Cell Differentiation - physiology | von Willebrand Factor - metabolism | Cell Line | Basic Helix-Loop-Helix Transcription Factors - genetics | DNA (Cytosine-5-)-Methyltransferase 1 | Endothelial Cells - metabolism | Cells, Cultured | Azacitidine - analogs & derivatives | Up-Regulation - genetics | DNA Methylation - genetics | Down-Regulation - genetics | Receptor, TIE-2 - genetics | Angiopoietin-1 - genetics | Azacitidine - pharmacology | Animals | Embryonic Stem Cells - drug effects | Cell Differentiation - drug effects | Endothelial Cells - cytology | Octamer Transcription Factor-3 - metabolism | CpG Islands - genetics | Mice | Sulfites | Endothelial growth factors | Immunocytochemistry | Leukemia | Embryonic stem cells | Gene expression | Endothelium | Stem cell research | Promoters (Genetics) | Methyltransferases | DNA | Genetic research | Bone morphogenetic proteins | Methylation | Genetics | Cellular biology | Rodents | Deoxyribonucleic acid--DNA | Stem cells | endothelial cells | embryonic stem cell
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2. Full Text Apelin gene therapy increases myocardial vascular density and ameliorates diabetic cardiomyopathy via upregulation of sirtuin 3
by Zeng, Heng and He, Xiaochen and Hou, Xuwei and Li, Lanfang and Chen, Jian-Xiong
American Journal of Physiology - Heart and Circulatory Physiology, ISSN 0363-6135, 02/2014, Volume 306, Issue 4, pp. H585 - H597
Microvascular insufficiency contributes to cardiac hypertrophy and worsens heart dysfunction in diabetic cardiomyopathy. Our recent study shows that apelin may... 
VEGF/VEGFR2 | Diabetic cardiomyopathy | Angiogenesis | Sirtuin 3 | Ang-1/Tie-2 | Apelin | NADPH OXIDASE | METABOLIC SYNDROME | CARDIAC & CARDIOVASCULAR SYSTEMS | PHYSIOLOGY | apelin | sirtuin 3 | angiogenesis | HEART-FAILURE | diabetic cardiomyopathy | TUMOR ANGIOGENESIS | PEPTIDE APELIN | IMPAIRED ANGIOGENESIS | CARDIAC-HYPERTROPHY | PERIPHERAL VASCULAR DISEASE | ORPHAN RECEPTOR APJ | EXPRESSION | ENDOTHELIAL GROWTH-FACTOR | Diabetic Cardiomyopathies - metabolism | Reactive Oxygen Species - metabolism | Sirtuin 3 - metabolism | Male | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | Vascular Endothelial Growth Factor A - genetics | Angiopoietin-2 - metabolism | Diabetic Cardiomyopathies - physiopathology | Receptors, Vascular Endothelial Growth Factor - metabolism | Myocardium - metabolism | Neovascularization, Pathologic - physiopathology | Receptor, TIE-2 - metabolism | Diabetic Cardiomyopathies - therapy | Receptors, Vascular Endothelial Growth Factor - genetics | Neovascularization, Pathologic - therapy | Heart - physiopathology | Sirtuin 3 - genetics | Endothelium, Vascular - physiopathology | Intercellular Signaling Peptides and Proteins - genetics | Up-Regulation - genetics | Adipokines | Receptor, TIE-2 - genetics | Diabetic Cardiomyopathies - genetics | Angiopoietin-1 - genetics | Animals | Endothelium, Vascular - metabolism | Neovascularization, Pathologic - genetics | Mice | Neovascularization, Pathologic - metabolism | Apoptosis - physiology | Prevention | Cardiomyopathy | Physiological aspects | Genetic research | Genetic aspects | Research | Diabetes | Gene therapy | Heart diseases | VEGFR2 | Tie-2 | VEGF | Ang-1 | Integrative Cardiovascular Physiology and Pathophysiology
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3. Full Text BAMBI Elimination Enhances Alternative TGF-beta Signaling and Glomerular Dysfunction in Diabetic Mice
by Fan, Y and Li, XZ and Xiao, WZ and Fu, J and Harris, RC and Lindenmeyer, M and Cohen, CD and Guillot, N and Baron, MH and Wang, NS and Lee, K and He, JC and Schlondorff, D and Chuang, PY
DIABETES, ISSN 0012-1797, 06/2015, Volume 64, Issue 6, pp. 2220 - 2233
BMP, activin, membrane-bound inhibitor (BAMBI) acts as a pseudo-receptor for the transforming growth factor (TGF)-beta type I receptor family and a negative... 
KIDNEY-DISEASE | CELLS | ACTIVATION | ANGIOGENESIS | ENDOCRINOLOGY & METABOLISM | ANTIBODY | MAJOR MEDIATOR | NEPHROPATHY | PROGRESSION | ENDOTHELIAL GROWTH-FACTOR | MATRIX GENE-EXPRESSION | Membrane Proteins - genetics | Humans | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Kidney Glomerulus - pathology | Angiopoietin-1 - metabolism | Blotting, Western | Vascular Endothelial Growth Factor Receptor-2 - genetics | Angiopoietin-1 - genetics | Animals | Smad5 Protein - metabolism | Smad1 Protein - genetics | Kidney Glomerulus - metabolism | Smad1 Protein - metabolism | Signal Transduction - physiology | Membrane Proteins - metabolism | Mice | Smad5 Protein - genetics | In Vitro Techniques | Transforming Growth Factor beta - metabolism | Glomerulonephritis | Type 2 diabetes | Genetically modified mice | Care and treatment | Usage | Activins | Research | Transforming growth factors | Life Sciences | Complications
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4. Full Text Mesenchymal Stem Cell Microvesicles Attenuate Acute Lung Injury in Mice Partly Mediated by Ang‐1 mRNA
by Tang, Xiao‐Dan and Shi, Lin and Monsel, Antoine and Li, Xiang‐Yang and Zhu, Hui‐Li and Zhu, Ying‐Gang and Qu, Jie‐Ming
STEM CELLS, ISSN 1066-5099, 07/2017, Volume 35, Issue 7, pp. 1849 - 1859
Microvesicles (MVs) derived from human mesenchymal stem cells (MSC MVs) were demonstrated to ameliorate inflammation in lungs. We have found their content of... 
Mesenchymal stem cell | Endothelial cell | Animal models | Lentiviral vector | Lung | SURVIVAL | PERMEABILITY | ALVEOLAR FLUID CLEARANCE | PROTECT | DELIVERY | CELL & TISSUE ENGINEERING | CELL BIOLOGY | BACTERIAL CLEARANCE | ONCOLOGY | BIOTECHNOLOGY & APPLIED MICROBIOLOGY | INFLAMMATION | SECRETION | ANGIOPOIETIN-1 GENE-THERAPY | STROMAL CELLS | HEMATOLOGY | Tumor Necrosis Factor-alpha - metabolism | RNA, Small Interfering - genetics | Humans | Tumor Necrosis Factor-alpha - genetics | Cell-Derived Microparticles - transplantation | Acute Lung Injury - genetics | Male | Cell-Derived Microparticles - chemistry | Angiopoietin-1 - metabolism | RNA, Messenger - metabolism | Capillary Permeability - genetics | Lipopolysaccharides | Mesenchymal Stromal Cells - cytology | Acute Lung Injury - prevention & control | Cell-Derived Microparticles - secretion | RNA, Messenger - antagonists & inhibitors | Chemokine CXCL2 - genetics | Interleukin-10 - metabolism | Lung - metabolism | Chemokine CXCL2 - metabolism | Neutrophils - metabolism | Disease Models, Animal | Neutrophils - pathology | Lung - pathology | Signal Transduction | Endothelial Cells - metabolism | Mice, Inbred C57BL | RNA, Messenger - genetics | Gene Expression Regulation | Mesenchymal Stromal Cells - secretion | Acute Lung Injury - pathology | Neutrophil Infiltration - genetics | Angiopoietin-1 - antagonists & inhibitors | Angiopoietin-1 - genetics | Animals | Acute Lung Injury - chemically induced | Endothelial Cells - cytology | Interleukin-10 - genetics | Mice | Bronchoalveolar Lavage Fluid - chemistry | Primary Cell Culture | RNA, Small Interfering - metabolism | Acute respiratory distress syndrome | Messenger RNA | Interleukins | Analysis | Stem cells | Permeability | Macrophages | Mitogens | Health aspects | Endothelium | Mesenchyme | Angiopoietin | Stabilization | Interleukin | Membrane permeability | Stem cell transplantation | Bronchoalveolar lavage | Rodents | Attenuation | Alveoli | Immunomodulation | Albumin | Bronchus | Leukocytes (neutrophilic) | Inflammation | Keratinocyte growth factor | Gene expression | Ribonucleic acid--RNA | Endothelial cells | Lungs | Tumor necrosis factor | Deterioration | Interleukin 10 | Microvasculature | In vitro methods and tests | Macrophage inflammatory protein | Integrity
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5. Full Text Consequences of chondrocyte hypertrophy on osteoarthritic cartilage: potential effect on angiogenesis
by Pesesse, L and Sanchez, C and Delcour, J.-P and Bellahcène, A and Baudouin, C and Msika, P and Henrotin, Y
Osteoarthritis and Cartilage, ISSN 1063-4584, 2013, Volume 21, Issue 12, pp. 1913 - 1923
Summary Objective The aim of this study was to investigate the link between the hypertrophic phenotype of chondrocytes and angiogenesis in osteoarthritis (OA)... 
Rheumatology | Angiogenesis | Bone sialoprotein | Chondrocyte hypertrophy | Osteoarthritis | RHEUMATOLOGY | METALLOPROTEINASES | OSTEOCHONDRAL JUNCTION | ARTICULAR-CARTILAGE | SIALOPROTEIN | ENDOTHELIAL-CELLS | GROWTH-FACTOR | BONE | DIFFERENTIATION | ORTHOPEDICS | EXPRESSION | ALGINATE BEADS | Osteopontin - genetics | Up-Regulation | Thrombospondins - genetics | Humans | Osteopontin - metabolism | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | Vascular Endothelial Growth Factor A - genetics | Osteoarthritis - physiopathology | Intercellular Signaling Peptides and Proteins - metabolism | Cartilage, Articular - metabolism | Thrombospondin 1 - genetics | Fibroblast Growth Factor 2 - metabolism | Neovascularization, Pathologic - physiopathology | Membrane Proteins - metabolism | Chondrocytes - metabolism | Endothelial Cells - physiology | Chondrocytes - pathology | Nerve Growth Factor - metabolism | Cartilage, Articular - cytology | Matrix Metalloproteinase 2 - metabolism | Membrane Proteins - genetics | Cells, Cultured | Gene Expression Regulation | Intercellular Signaling Peptides and Proteins - genetics | Osteoarthritis - metabolism | Nerve Growth Factor - genetics | Reverse Transcriptase Polymerase Chain Reaction | Cell Adhesion | Osteoarthritis - genetics | Angiopoietin-1 - genetics | Matrix Metalloproteinase 2 - genetics | Fibroblast Growth Factor 2 - genetics | Integrin-Binding Sialoprotein - genetics | Neovascularization, Pathologic - genetics | Neovascularization, Pathologic - metabolism | Thrombospondin 1 - metabolism | Integrin-Binding Sialoprotein - metabolism | Thrombospondins - metabolism | Cell Movement | Hypertrophy
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6. Full Text Linking transgene expression of engineered mesenchymal stem cells and angiopoietin-1-induced differentiation to target cancer angiogenesis
by Conrad, Claudius and Hüsemann, Yves and Niess, Hanno and Von Luettichau, Irene and Huss, Ralf and Bauer, Christian and Jauch, Karl-Walter and Klein, Christoph A and Bruns, Christiane and Nelson, Peter J
Annals of Surgery, ISSN 0003-4932, 03/2011, Volume 253, Issue 3, pp. 566 - 571
Objective: To specifically target tumor angiogenesis by linking transgene expression of engineered mesenchymal stem cells to angiopoietin-1-induced... 
SURGERY | GENE | GLIOMA | GROWTH | TISSUE | VECTORS | DELIVERY | Adenocarcinoma - pathology | Receptor, TIE-2 | Gene Expression - genetics | Mammary Neoplasms, Experimental - genetics | Neovascularization, Pathologic - pathology | Cell Transformation, Neoplastic - genetics | Mammary Neoplasms, Experimental - pathology | Female | Adenocarcinoma - genetics | Angiopoietin-1 - pharmacology | Gene Targeting | Genes, Transgenic, Suicide - genetics | Thymidine Kinase - genetics | Mice, Inbred C57BL | Pancreatic Neoplasms - pathology | Simplexvirus - genetics | Transgenes - genetics | Mesenchymal Stromal Cells - metabolism | Genes, Reporter - genetics | Mice, Transgenic | Pancreatic Neoplasms - genetics | Animals | Genetic Engineering | Receptor Protein-Tyrosine Kinases - genetics | Neovascularization, Pathologic - genetics | Mice | Mice, Inbred BALB C | Cell Transformation, Neoplastic - pathology | Mesenchymal Stem Cell Transplantation | Genetic Therapy - methods | Index Medicus | Abridged Index Medicus
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7. Full Text Genetic Risk Factors for Portopulmonary Hypertension in Patients with Advanced Liver Disease
by Roberts, Kari E and Fallon, Michael B and Krowka, Michael J and Brown, Robert S and Trotter, James F and Peter, Inga and Tighiouart, Hocine and Knowles, James A and Rabinowitz, Daniel and Benza, Raymond L and Badesch, David B and Taichman, Darren B and Horn, Evelyn M and Zacks, Steven and Kaplowitz, Neil and Kawut, Steven M and Pulmonary Vascular Complications of Liver Disease Study Group and Pulm Vasc Complications Liver Dis and Pulmonary Vascular Complications of Liver Disease Study Group
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 05/2009, Volume 179, Issue 9, pp. 835 - 842
Rationale: Portopulmonary hypertension (PPHTN) occurs in 6% of liver transplant candidates. The pathogenesis of this complication of portal hypertension is... 
Hypertension | Pulmonary | Genetic polymorphism | Portal hypertension | SURVIVAL | SEROTONIN TRANSPORTER | portal hypertension | PULMONARY ARTERIAL-HYPERTENSION | hypertension, pulmonary | ANGIOPOIETIN-1 | BETA | TRANSPLANTATION | RESPIRATORY SYSTEM | ESTROGEN-RECEPTOR-ALPHA | ESTRADIOL | genetic polymorphism | EXPRESSION | ASSOCIATION | CRITICAL CARE MEDICINE | Estradiol - blood | Hypertension, Portal - genetics | Humans | Middle Aged | Risk Factors | Genotype | Male | Case-Control Studies | Receptors, Retinoic Acid - genetics | Angiopoietin-1 - genetics | Aromatase - genetics | Estrogen Receptor alpha - genetics | Cyclic Nucleotide Phosphodiesterases, Type 5 - genetics | Liver Diseases - complications | Female | Polymorphism, Single Nucleotide | Calcium-Binding Proteins - genetics | F. Pulmonary Vascular Disease
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8. Effects of angiopoietin-1 on inflammatory injury in endothelial progenitor cells and blood vessels
by Wang, Yi-Qing and Song, Jing-Jin and Han, Xiao and Liu, Yi-Ye and Wang, Xi-Huang and Li, Zhi-ming and Tzeng, Chi-Meng
Current Gene Therapy, ISSN 1566-5232, 2014, Volume 14, Issue 2, pp. 128 - 135
Endothelial progenitor cells (EPCs) and angiopoietin-1 (Ang-1) play important roles in vasculogenesis and angiogenesis, respectively. Thus, targeting both... 
Angiopoietin-1 | Inflammation | Carotid balloon catheter injury | Endothelial progenitor cells | VASCULAR REGENERATION | ANGIOGENESIS | RAT | MYOCARDIAL REPAIR | NEOINTIMAL HYPERPLASIA | ARTERIES | THERAPY | inflammation | endothelial progenitor cells | GENETICS & HEREDITY | GENE-TRANSFER | carotid balloon catheter injury | EXPRESSION | Tumor Necrosis Factor-alpha - metabolism | Blood Vessels - metabolism | Tumor Necrosis Factor-alpha - genetics | Cell Survival - genetics | Male | Neovascularization, Pathologic - virology | Angiopoietin-1 - metabolism | Inflammation - metabolism | Endothelial Progenitor Cells - virology | Proliferating Cell Nuclear Antigen - genetics | Blood Vessels - virology | Lentivirus - genetics | Vascular Cell Adhesion Molecule-1 - genetics | Endothelial Progenitor Cells - metabolism | Cells, Cultured | Inflammation - virology | Rats | Rats, Sprague-Dawley | Genetic Vectors - genetics | Angiopoietin-1 - genetics | Intercellular Adhesion Molecule-1 - metabolism | Animals | Intercellular Adhesion Molecule-1 - genetics | Inflammation - genetics | Neovascularization, Pathologic - genetics | Neovascularization, Pathologic - metabolism | Transcription, Genetic - genetics | Proliferating Cell Nuclear Antigen - metabolism | Vascular Cell Adhesion Molecule-1 - metabolism | Genetic Therapy - methods
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9. Full Text Angiopoietin-1/Tie2 signal augments basal notch signal controlling vascular quiescence by inducing delta-like 4 expression through AKT-mediated activation of β-catenin
by Zhang, Jianghui and Fukuhara, Shigetomo and Sako, Keisuke and Takenouchi, Takato and Kitani, Hiroshi and Kume, Tsutomu and Koh, Gou Young and Mochizuki, Naoki
Journal of Biological Chemistry, ISSN 0021-9258, 03/2011, Volume 286, Issue 10, pp. 8055 - 8066
Angiopoietin-1 (Ang1) regulates both vascular quiescence and angiogenesis through the receptor tyrosine kinase Tie2. We and another group previously showed... 
CELL-CELL | DLL4 | MATRIX | ANGIOGENESIS | PATHWAY | VEGF | BIOCHEMISTRY & MOLECULAR BIOLOGY | VESSEL FORMATION | LIGAND | INHIBITS TUMOR-GROWTH | TIE2 RECEPTOR | Phosphorylation - physiology | Receptors, Notch - metabolism | Extracellular Matrix - metabolism | Glycogen Synthase Kinase 3 beta | Receptors, Notch - genetics | Phosphatidylinositol 3-Kinases - metabolism | Angiopoietin-1 - metabolism | Proto-Oncogene Proteins c-akt - genetics | beta Catenin - biosynthesis | Extracellular Matrix - genetics | Intercellular Signaling Peptides and Proteins - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Umbilical Veins - cytology | Endothelial Cells - metabolism | Intercellular Signaling Peptides and Proteins - genetics | Gene Expression Regulation - physiology | Glycogen Synthase Kinase 3 - metabolism | Receptor Protein-Tyrosine Kinases - metabolism | beta Catenin - genetics | Phosphatidylinositol 3-Kinases - genetics | Angiopoietin-1 - genetics | Neovascularization, Physiologic - physiology | Glycogen Synthase Kinase 3 - genetics | Receptor Protein-Tyrosine Kinases - genetics | Endothelial Cells - cytology | Signal Transduction - physiology | Umbilical Veins - metabolism | Δ-Like 4 | Signal Transduction | Extracellular Matrix Proteins | Tie2 | Vascular Quiescence | Angiopoietin-1 | β-Catenin | Glycogen Synthase Kinase 3 | Notch Pathway | AKT PKB | Endothelium
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10. Full Text Constitutive association of Tie1 and Tie2 with endothelial integrins is functionally modulated by angiopoietin-1 and fibronectin
by Dalton, Annamarie C and Shlamkovitch, Tomer and Papo, Niv and Barton, William A
PLoS ONE, ISSN 1932-6203, 10/2016, Volume 11, Issue 10, p. e0163732
Functional cross-talk between Tie2 and Integrin signaling pathways is essential to coordinate endothelial cell adhesion and migration in response to the... 
Cell Adhesion - genetics | Integrin alpha5beta1 - genetics | Phosphorylation | Endothelial Cells - metabolism | Humans | Vesicular Transport Proteins - genetics | Extracellular Matrix - metabolism | Receptor, TIE-1 - metabolism | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | Vascular Endothelial Growth Factor A - genetics | Fibronectins - metabolism | Integrin alphaVbeta3 - metabolism | Receptor, TIE-2 - genetics | Angiopoietin-1 - genetics | Extracellular Matrix - genetics | MAP Kinase Signaling System - genetics | Integrin alphaVbeta3 - genetics | Fluorescence Resonance Energy Transfer | Protein Binding | Receptor, TIE-2 - metabolism | Fibronectins - genetics | Integrin alpha5beta1 - metabolism | Receptor, TIE-1 - genetics | Fibronectins | Integrins | Endothelium | Biotechnology | Angiopoietin | Biochemistry | Kinases | Cell surface | Fibronectin | Cell adhesion & migration | Proteins | Angiogenesis | Cascades | Rodents | Atherosclerosis | Cell adhesion | Extracellular matrix | Physiology | Fluorescence resonance energy transfer | Localization | Vascular endothelial growth factor | Binding | Extracellular signal-regulated kinase | MAP kinase | Endothelial cells | Signaling | Ligands | Molecular biology | Cell migration | Recognition
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11. Full Text Hypoxia-inducible hydrogels
by Park, Kyung Min and Gerecht, Sharon
Nature Communications, ISSN 2041-1723, 06/2014, Volume 5, Issue 1, p. 4075
Oxygen is vital for the existence of all multicellular organisms, acting as a signalling molecule regulating cellular activities. Specifically, hypoxia, which... 
PLURIPOTENT STEM-CELLS | OXYGEN | ANGIOGENESIS | REGENERATION | MULTIDISCIPLINARY SCIENCES | IN-VIVO | DEGRADATION | EXTRACELLULAR-MATRIX | BIOMATERIALS | EXPRESSION | VASCULAR MORPHOGENESIS | Matrix Metalloproteinases - genetics | Humans | Gene Expression Profiling | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | Vascular Endothelial Growth Factor A - genetics | Oxygen - metabolism | Vascular Endothelial Growth Factor Receptor-2 - genetics | Basic Helix-Loop-Helix Transcription Factors - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Computer Simulation | Hydrogels - metabolism | Wound Healing - genetics | Gelatin - chemistry | Laccase | Basic Helix-Loop-Helix Transcription Factors - genetics | Endothelial Cells - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Neovascularization, Physiologic - genetics | Oxygen Consumption | Cellular Microenvironment | Vascular Endothelial Growth Factor Receptor-2 - metabolism | Angiopoietin-1 - genetics | Neovascularization, Physiologic - physiology | Biocompatible Materials | Matrix Metalloproteinases - metabolism | Coumaric Acids
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12. Full Text Germline genetic variants in TEK, ANGPT1, ANGPT2, MMP9, FGF2 and VEGFA are associated with pathologic complete response to bevacizumab in breast cancer patients
by Makhoul, Issam and Todorova, Valentina K and Siegel, Eric R and Erickson, Stephen W and Dhakal, Ishwori and Raj, Vinay R and Lee, Jeannette Y and Orloff, Mohammed S and Griffin, Robert J and Henry-Tillman, Ronda S and Klimberg, Suzanne and Hutchins, Laura F and Kadlubar, Susan A
PLoS ONE, ISSN 1932-6203, 01/2017, Volume 12, Issue 1, p. e0168550
Background We previously reported improved pathologic complete response (pCR) in a prospective phase II study using neoadjuvant bevacizumab in combination with... 
MULTIDISCIPLINARY SCIENCES | Bevacizumab - therapeutic use | Prospective Studies | Angiopoietin-2 - genetics | Humans | Middle Aged | Male | Vascular Endothelial Growth Factor A - genetics | Ethnic Groups | Matrix Metalloproteinase 9 - genetics | Observational Studies as Topic | Adult | Female | Neoadjuvant Therapy | Breast Neoplasms - ethnology | Gene Frequency | Genotype | Treatment Outcome | Breast Neoplasms - drug therapy | Receptor, TIE-2 - genetics | Angiopoietin-1 - genetics | Regression Analysis | Breast Neoplasms - genetics | Fibroblast Growth Factor 2 - genetics | Neovascularization, Pathologic - genetics | Aged | Polymorphism, Single Nucleotide | Clinical Trials, Phase II as Topic | Care and treatment | Drug metabolism | Development and progression | Genetic aspects | Breast cancer | Single nucleotide polymorphisms | Health aspects | Fibroblast growth factor | Angiopoietin | Genes | Oncology | Systematic review | Single-nucleotide polymorphism | Metastasis | Matrix metalloproteinase | Cancer therapies | Bevacizumab | Angiogenesis | Regression models | Race | Metalloproteinase | Vascular endothelial growth factor | Protein-tyrosine kinase | Genotypes | Deoxyribonucleic acid--DNA | Fibroblast growth factor 2 | Tyrosine | Hematology | Heredity | FDA approval | Regression analysis | Patients | Survival | Gelatinase B | Polymerase chain reaction | Studies | Genetic variance | Chemotherapy | Genotyping | Gene frequency | Biomarkers | Cancer | Deoxyribonucleic acid | DNA
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13. Full Text Extracellular vesicle miR-7977 is involved in hematopoietic dysfunction of mesenchymal stromal cells via poly(rC) binding protein 1 reduction in myeloid neoplasms
by Horiguchi, Hiroto and Kobune, Masayoshi and Kikuchi, Shohei and Yoshida, Masahiro and Murata, Masaki and Murase, Kazuyuki and Iyama, Satoshi and Takada, Kohichi and Sato, Tsutomu and Ono, Kaoru and Hashimoto, Akari and Tatekoshi, Ayumi and Kamihara, Yusuke and Kawano, Yutaka and Miyanishi, Koji and Sawada, Norimasa and Kato, Junji
Haematologica, ISSN 0390-6078, 03/2016, Volume 101, Issue 4, pp. 437 - 447
The failure of normal hematopoiesis is observed in myeloid neoplasms. However, the precise mechanisms governing the replacement of normal hematopoietic stem... 
EX-VIVO EXPANSION | PROGENITOR CELLS | FAS LIGAND | STEM-CELLS | ACUTE MYELOGENOUS LEUKEMIA | BONE-MARROW NICHE | IN-VIVO | EXOSOMES | HEMATOLOGY | MYELODYSPLASTIC SYNDROME | EXPRESSION | Lymphoma - physiopathology | Extracellular Vesicles - chemistry | Jagged-1 Protein - metabolism | Coculture Techniques | Humans | Leukemia, Myeloid, Acute - metabolism | Gene Expression Regulation, Neoplastic | MicroRNAs - metabolism | Gene Expression Profiling | Stem Cell Factor - genetics | Angiopoietin-1 - metabolism | Extracellular Vesicles - metabolism | Lymphoma - metabolism | Molecular Mimicry | Transfection | Oligoribonucleotides - metabolism | Myelodysplastic Syndromes - metabolism | Myelodysplastic Syndromes - physiopathology | Stem Cell Factor - metabolism | Signal Transduction | Extracellular Vesicles - pathology | Bone Marrow Cells - pathology | Heterogeneous-Nuclear Ribonucleoproteins - metabolism | Lymphoma - genetics | Mesenchymal Stromal Cells - metabolism | Hematopoiesis - genetics | Jagged-1 Protein - genetics | Heterogeneous-Nuclear Ribonucleoproteins - genetics | Angiopoietin-1 - genetics | MicroRNAs - genetics | Myelodysplastic Syndromes - genetics | Mesenchymal Stromal Cells - pathology | Primary Cell Culture | Neoplasm Staging | Bone Marrow Cells - metabolism | Leukemia, Myeloid, Acute - physiopathology | Leukemia, Myeloid, Acute - genetics | Oligoribonucleotides - genetics
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14. Full Text Hematopoietic stem and progenitor cells regulate the regeneration of their niche by secreting Angiopoietin-1
by Zhou, Bo O and Ding, Lei and Morrison, Sean J
eLife, ISSN 2050-084X, 03/2015, Volume 2015, Issue 4, p. e05521
Hematopoietic stem cells (HSCs) are maintained by a perivascular niche in bone marrow but it is unclear whether the niche is reciprocally regulated by HSCs.... 
LONG-TERM | OVEREXPRESSING ANGIOPOIETIN-1 | SINUSOIDAL ENDOTHELIAL-CELLS | BONE-MARROW NICHE | BIOLOGY | SELF-RENEWAL | LYMPHOID PROGENITORS | MICE | DISTINCT ROLES | RECEPTOR TYROSINE KINASE | TIE2 RECEPTOR | Gamma Rays | Stem Cell Niche - radiation effects | Receptors, Leptin - genetics | Blood Vessels - metabolism | Male | Angiopoietin-1 - metabolism | Proto-Oncogene Proteins c-kit - metabolism | Capillary Permeability - radiation effects | Regeneration - radiation effects | Blood Vessels - radiation effects | Hematopoiesis - radiation effects | Regeneration - genetics | Nestin - genetics | Female | Integrases - metabolism | Proto-Oncogene Proteins c-kit - genetics | Osteoblasts - cytology | Megakaryocytes - cytology | Megakaryocytes - metabolism | Megakaryocytes - radiation effects | Hematopoietic Stem Cells - radiation effects | Stem Cell Niche - genetics | Osteoblasts - radiation effects | Signal Transduction | Bone Marrow Cells - cytology | Stromal Cells - metabolism | Gene Expression Regulation | Hematopoiesis - genetics | Mice, Transgenic | Hematopoietic Stem Cells - metabolism | Bone Marrow Cells - radiation effects | Blood Vessels - cytology | Nestin - metabolism | Angiopoietin-1 - genetics | Animals | Hematopoietic Stem Cells - cytology | Mice | Receptors, Leptin - metabolism | Osteoblasts - metabolism | Integrases - genetics | Bone Marrow Cells - metabolism | Stromal Cells - cytology | Stromal Cells - radiation effects | Angiopoietin | Radiation | Stem cell transplantation | Osteoblasts | c-Kit protein | Experiments | Hematopoietic stem cells | Endothelial cells | Stains & staining | Regeneration | Angiogenesis | Allografts | Clonal deletion | Microscopy | Stromal cells | Rodents | Stem cells | Bone marrow | Megakaryocytes
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