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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
Journal Article
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
Journal Article
Journal Article
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
Journal Article
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
Journal Article
Journal Article
American Journal of Respiratory and Critical Care Medicine, ISSN 1073-449X, 05/2009, Volume 179, Issue 9, pp. 835 - 842
Journal Article
Current Gene Therapy, ISSN 1566-5232, 2014, Volume 14, Issue 2, pp. 128 - 135
Journal Article
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
Journal Article
PLoS ONE, ISSN 1932-6203, 10/2016, Volume 11, Issue 10, p. e0163732
Journal Article
Journal Article
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
Journal Article
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
Journal Article
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
Journal Article