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1. Full Text Propranolol inhibition of β-adrenergic receptor does not suppress pathologic neovascularization in oxygen-induced retinopathy
by Chen, Jing and Joyal, Jean-Sebastian and Hatton, Colman J and Juan, Aimee M and Pei, Dorothy T and Hurst, Christian G and Xu, Dan and Stahl, Andreas and Hellstrom, Ann and Smith, Lois E H and Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering and Sahlgrenska akademin and Göteborgs universitet and Gothenburg University and Sahlgrenska Academy and Institute of Neuroscience and Physiology, Department of Clinical Neuroscience and Rehabilitation
Investigative ophthalmology & visual science, ISSN 0146-0404, 2012, Volume 53, Issue 6, pp. 2968 - 2977
PURPOSE. Retinopathy of prematurity (ROP) is a leading cause of blindness in children and is, in its most severe form, characterized by uncontrolled growth of... 
RETINAL NEOVASCULARIZATION | BLOCKERS | MOUSE MODEL | RAT RETINA | OPHTHALMOLOGY | INFANTILE HEMANGIOMAS | FACTOR EXPRESSION | PREMATURITY | INFANCY | ENDOTHELIAL GROWTH-FACTOR | Disease Models | Up-Regulation | Other Medical Sciences | Cell Proliferation | Endothelial Cells/drug effects | Oxygen/toxicity | Humans | Drug Evaluation | Vascular Endothelial Growth Factor A/genetics/metabolism | Infant | Propranolol/administration & dosage | Gene Expression Profiling | Adrenergic | Oral | Intraperitoneal | RNA/metabolism | Receptors | Retinopathy of Prematurity/metabolism/prevention & control | beta/metabolism | Preclinical | Adrenergic beta-Antagonists/administration & dosage | Drug | Administration | Retinal Neovascularization/metabolism/prevention & control | Enzyme-Linked Immunosorbent Assay | Subcutaneous | Angiopoietin-2/genetics/metabolism | Erythropoietin/genetics/metabolism | Reverse Transcriptase Polymerase Chain Reaction | Retina/cytology | Angiopoietin-1/genetics/metabolism | Injections | Animals | Newborn | Annan medicin och hälsovetenskap | Animal | Dose-Response Relationship | Mice | Vascular Endothelial Growth Factor/genetics/metabolism
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2. 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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3. Full Text Uterine natural killer cells initiate spiral artery remodeling in human pregnancy
by Robson, Andrew and Harris, Lynda K and Innes, Barbara A and Lash, Gendie E and Aljunaidy, Mais M and Aplin, John D and Baker, Philip N and Robson, Stephen C and Bulmer, Judith N
FASEB Journal, ISSN 0892-6638, 12/2012, Volume 26, Issue 12, pp. 4876 - 4885
Uterine spiral artery remodeling is required for successful human pregnancy; impaired remodeling is associated with pregnancy complications, including late... 
Proteases | Vascular smooth muscle cells | Angiogenic growth factors | TROPHOBLAST INVASION | GRANULATED LYMPHOCYTES | BIOCHEMISTRY & MOLECULAR BIOLOGY | proteases | CELL BIOLOGY | angiogenic growth factors | EXTRAVILLOUS TROPHOBLAST | SMOOTH-MUSCLE | IN-VITRO | BIOLOGY | CARDIOVASCULAR-DISEASE | MATERNAL ARTERIES | GROWTH-FACTOR | vascular smooth muscle cells | EXPRESSION | FACTS | Immunohistochemistry | Muscle, Smooth, Vascular - metabolism | Decidua - cytology | Humans | Extracellular Matrix - metabolism | Culture Media, Conditioned - pharmacology | Interferon-gamma - metabolism | Angiopoietin-1 - metabolism | Angiopoietin-2 - pharmacology | Angiopoietin-2 - metabolism | Uterine Artery - physiology | Placenta - cytology | Myometrium - metabolism | Female | Trophoblasts - cytology | Uterine Artery - drug effects | Myocytes, Smooth Muscle - drug effects | Uterus - blood supply | Myocytes, Smooth Muscle - metabolism | Angiopoietin-1 - pharmacology | Cell Line | Trophoblasts - metabolism | Uterine Artery - cytology | Tissue Culture Techniques | Extracellular Matrix - drug effects | Cells, Cultured | Muscle, Smooth, Vascular - cytology | Killer Cells, Natural - physiology | Decidua - metabolism | Myometrium - cytology | Placenta - metabolism | Pregnancy | Trophoblasts - physiology | Vascular Endothelial Growth Factor C - metabolism | Uterus - cytology | Killer Cells, Natural - metabolism | Interferon-gamma - pharmacology | Culture Media, Conditioned - metabolism | Vascular Endothelial Growth Factor C - pharmacology
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4. Full Text Overexpression of angiopoietin-1 increases CD133+/c-kit+ cells and reduces myocardial apoptosis in db/db mouse infarcted hearts
by Zeng, Heng and Li, Lanfang and Chen, Jian-Xiong
PLoS ONE, ISSN 1932-6203, 04/2012, Volume 7, Issue 4, p. e35905
Hematopoietic progenitor CD133(+)/c-kit(+) cells have been shown to be involved in myocardial healing following myocardial infarction (MI). Previously we... 
CD31(+) CELLS | ENDOTHELIAL PROGENITOR CELLS | ISCHEMIA/REPERFUSION INJURY | ACTIVATION | ISCHEMIC VASCULAR-DISEASE | ANGIOGENIC ACTIVITY | BONE-MARROW | BIOLOGY | RECEPTOR | TOPCARE-AMI | EXPRESSION | Up-Regulation | Capillaries - pathology | Receptors, Notch - metabolism | Cardiomegaly - pathology | Angiopoietin-1 - metabolism | Antigens, CD - metabolism | Peptides - metabolism | Serrate-Jagged Proteins | Bone Marrow - metabolism | Myocardium - metabolism | Endomyocardial Fibrosis - complications | Myocardial Infarction - physiopathology | Capillaries - metabolism | Apelin | Jagged-1 Protein | Capillaries - physiopathology | Signal Transduction | Cardiomegaly - physiopathology | Myocardial Infarction - metabolism | Receptors, CXCR4 - metabolism | Chemokine CXCL12 - metabolism | Hematopoietic Stem Cells - cytology | Endomyocardial Fibrosis - metabolism | Mice | Diabetes Mellitus, Type 2 - pathology | Cardiomegaly - metabolism | Cell Movement | Actins - metabolism | Glycoproteins - metabolism | Diabetes Mellitus, Type 2 - metabolism | Proto-Oncogene Proteins c-kit - metabolism | Intercellular Signaling Peptides and Proteins - metabolism | Platelet Endothelial Cell Adhesion Molecule-1 - metabolism | Myocardial Infarction - pathology | Endomyocardial Fibrosis - pathology | Membrane Proteins - metabolism | Heart Function Tests | Diabetes Mellitus, Type 2 - complications | Calcium-Binding Proteins - metabolism | Myocardium - pathology | Adipokines | AC133 Antigen | Cardiomegaly - complications | Myocardial Infarction - complications | Animals | Diabetes Mellitus, Type 2 - physiopathology | Bone Marrow - pathology | Receptor, Notch3 | Endomyocardial Fibrosis - physiopathology | Apoptosis | Advertising executives | Vascular endothelial growth factor | Adenoviruses | Heart attack | Myocardial infarction | Heart | Diabetic retinopathy | Heart attacks | Angiopoietin | Recovery of function | Smooth muscle | Cardiovascular disease | Recruitment | Angiogenesis | Toxicology | Cell growth | Ischemia | Data recovery | Rodents | Bone marrow | Repair | Heart diseases | Immunoglobulins | Diabetes mellitus | Coronary artery | Muscles | Pharmacology | c-Kit protein | Hemopoiesis | Studies | Ostomy | Coronary vessels | Fibrosis | Stem cells | Myocardium | Infarction | Diabetes | Laboratory animals
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5. Full Text Stimulating the Neurotrophic and Angiogenic Properties of Human Adipose-Derived Stem Cells Enhances Nerve Repair
by Kingham, Paul J and Kolar, Mallappa K and Novikova, Liudmila N and Novikov, Lev N and Wiberg, Mikael and Medicinska fakulteten and Institutionen för integrativ medicinsk biologi (IMB) and Handkirurgi and Institutionen för kirurgisk och perioperativ vetenskap and Umeå universitet and Anatomi
Stem Cells and Development, ISSN 1547-3287, 04/2014, Volume 23, Issue 7, pp. 741 - 754
In future, adipose-derived stem cells (ASC) might be used to treat neurological disorders. In this study, the neurotrophic and angiogenic properties of human... 
Original Research Reports | MEDICINE, RESEARCH & EXPERIMENTAL | AXONAL REGENERATION | ROOT GANGLIA NEURONS | TRANSCRIPTION FACTOR-3 ATF3 | SENSORY NEURONS | CELL & TISSUE ENGINEERING | TRANSPLANTATION | C-JUN PHOSPHORYLATION | IN-VITRO | NEURITE OUTGROWTH | GROWTH-FACTOR | SCHWANN-CELLS | STROMAL CELLS | HEMATOLOGY | Brain-Derived Neurotrophic Factor - genetics | Spinal Cord - metabolism | Humans | Nerve Regeneration - physiology | Adipose Tissue - cytology | Adipocytes - cytology | Culture Media, Conditioned - pharmacology | JNK Mitogen-Activated Protein Kinases - metabolism | Neurons - cytology | Ganglia, Spinal - cytology | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | GAP-43 Protein - genetics | Vascular Endothelial Growth Factor A - genetics | Stem Cell Transplantation | Adipose Tissue - metabolism | Glial Cell Line-Derived Neurotrophic Factor - metabolism | Mesenchymal Stromal Cells - cytology | Adult | Brain-Derived Neurotrophic Factor - metabolism | Cell Differentiation | Neurons - metabolism | JNK Mitogen-Activated Protein Kinases - genetics | Spinal Cord - cytology | Activating Transcription Factor 3 - genetics | Biomarkers - metabolism | Mesenchymal Stromal Cells - drug effects | Gene Expression | GAP-43 Protein - metabolism | Glial Cell Line-Derived Neurotrophic Factor - genetics | Mesenchymal Stromal Cells - metabolism | Rats | Activating Transcription Factor 3 - metabolism | Cell Lineage - physiology | Angiopoietin-1 - genetics | Animals | Adipocytes - metabolism | Adipocytes - transplantation | Adipose Tissue - drug effects | Neovascularization, Physiologic | Ganglia, Spinal - metabolism | Adipose tissues | Nervous system diseases | Care and treatment | Prognosis | Physiological aspects | Development and progression | Research | Neovascularization | Gene expression | Risk factors | Basic Medicine | Neurosciences | Medical and Health Sciences | Medicin och hälsovetenskap | Medicinska och farmaceutiska grundvetenskaper | Neurovetenskaper
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6. Full Text Peroxisome proliferator-activated receptor alpha agonist suppresses neovascularization by reducing both vascular endothelial growth factor and angiopoietin-2 in corneal alkali burn
by Arima, Takeshi and Uchiyama, Masaaki and Nakano, Yuichiro and Nagasaka, Shinya and Kang, Dedong and Shimizu, Akira and Takahashi, Hiroshi
Scientific Reports, ISSN 2045-2322, 12/2017, Volume 7, Issue 1, pp. 17763 - 11
We investigated the effect of a peroxisome proliferator-activated receptor alpha (PPAR?alpha) agonist ophthalmic solution in wound healing using a rat corneal... 
GAMMA | PPAR-ALPHA | CELLS | LIPID-METABOLISM | COLLAGEN | TIE2 | INFLAMMATION | MULTIDISCIPLINARY SCIENCES | FACTOR-KAPPA-B | EXPRESSION | BASEMENT-MEMBRANE | Eye Burns - drug therapy | Ophthalmic Solutions - pharmacology | Burns, Chemical - metabolism | Corneal Neovascularization - drug therapy | Collagen Type III - metabolism | Male | Angiopoietin-1 - metabolism | RNA, Messenger - metabolism | Angiopoietin-2 - metabolism | Corneal Injuries - metabolism | Myofibroblasts - metabolism | Cicatrix - metabolism | Fenofibrate - pharmacology | Cornea - drug effects | Alkalies - pharmacology | Neutrophils - metabolism | Wound Healing - drug effects | Disease Models, Animal | Endothelial Cells - metabolism | Neutrophils - drug effects | Rats | Myofibroblasts - drug effects | Up-Regulation - drug effects | Cornea - metabolism | Cicatrix - drug therapy | Macrophages - metabolism | Animals | Corneal Neovascularization - metabolism | Neovascularization, Pathologic - drug therapy | Burns, Chemical - drug therapy | Eye Burns - metabolism | Macrophages - drug effects | PPAR alpha - agonists | Vascular Endothelial Growth Factors - metabolism | Neovascularization, Pathologic - metabolism | Corneal Injuries - drug therapy | Cornea | Wound healing | Angiopoietin | Stroma | Collagen (type III) | Leukocytes (neutrophilic) | Inflammation | Gene expression | Macrophages | Endothelial cells | Vascularization | Fenofibrate | Rodents | Vascular endothelial growth factor
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7. Full Text Deletion of placental growth factor prevents diabetic retinopathy and is associated with akt activation and HIF1α-VEGF pathway inhibition
by Huang, Hu and He, Jianbo and Johnson, Da'kuawn and Wei, Yanhong and Liu, Ying and Wang, Shuang and Lutty, Gerard A and Duh, Elia J and Semba, Richard D
Diabetes, ISSN 0012-1797, 01/2015, Volume 64, Issue 1, pp. 200 - 212
A new diabetic mouse strain, the Akita.PlGF knockout ((-/-)), was generated to study the role of placental growth factor (PlGF) in the pathogenesis of diabetic... 
PATHOGENESIS | FACTOR B | CELLS | VEGF | ENDOCRINOLOGY & METABOLISM | GENE-EXPRESSION | MICE | ANGIOPOIETIN-1 | VASCULAR-PERMEABILITY | NEOVASCULARIZATION | BREAKDOWN | Cadherins - metabolism | Capillaries - pathology | Pregnancy Proteins - genetics | Male | Pregnancy Proteins - metabolism | Vascular Endothelial Growth Factor A - metabolism | Antigens, CD - metabolism | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Pericytes - pathology | Female | Neovascularization, Pathologic - prevention & control | Zonula Occludens-1 Protein - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Capillaries - metabolism | Disease Models, Animal | Mice, Inbred C57BL | Pericytes - metabolism | Diabetic Retinopathy - metabolism | Diabetic Retinopathy - genetics | Mice, Knockout | Diabetic Retinopathy - prevention & control | Animals | Placenta Growth Factor | Neovascularization, Pathologic - genetics | Signal Transduction - physiology | Neovascularization, Pathologic - metabolism | Apoptosis - physiology | Blood Glucose - metabolism | Body Weight - physiology | Complications
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8. Full Text A new blood–brain barrier model using primary rat brain endothelial cells, pericytes and astrocytes
by Nakagawa, Shinsuke and Deli, Mária A and Kawaguchi, Hiroko and Shimizudani, Takeshi and Shimono, Takanori and Kittel, Ágnes and Tanaka, Kunihiko and Niwa, Masami
Neurochemistry International, ISSN 0197-0186, 2009, Volume 54, Issue 3, pp. 253 - 263
Blood–brain barrier (BBB) characteristics are induced and maintained by cross-talk between brain microvessel endothelial cells and neighbouring elements of the... 
Astrocytes | Pericytes | In vitro BBB model (rat) | Tight junction | Transendothelial electrical resistance | Co-culture | P-Glycoprotein | Drug permeability | Blood–brain barrier | Brain endothelial cells | Blood-brain barrier | DRUG | PERMEABILITY | BIOCHEMISTRY & MOLECULAR BIOLOGY | ANGIOPOIETIN-1 | INDUCTION | GLIAL-CELLS | NEUROSCIENCES | MESSENGER-RNA | IN-VITRO MODEL | CULTURES | EXPRESSION | ATP-Binding Cassette, Sub-Family B, Member 1 - metabolism | Pericytes - ultrastructure | Phosphoproteins - metabolism | Blood-Brain Barrier - ultrastructure | Occludin | Microcirculation - physiology | Endothelial Cells - ultrastructure | Membrane Proteins - metabolism | Capillaries - metabolism | Rhodamine 123 - pharmacokinetics | Tight Junctions - metabolism | Microscopy, Electron, Transmission | Capillaries - ultrastructure | Endothelial Cells - metabolism | Pericytes - metabolism | Cells, Cultured | Rats | Claudin-5 | Cerebral Arteries - ultrastructure | Membrane Potentials - physiology | Blood-Brain Barrier - metabolism | Astrocytes - ultrastructure | Tight Junctions - ultrastructure | Animals | Carrier Proteins - metabolism | Zonula Occludens-1 Protein | Cell Membrane Permeability - physiology | Cerebral Arteries - metabolism | Models, Biological | Cell Membrane Permeability - drug effects | ATP Binding Cassette Transporter, Sub-Family B - metabolism | Astrocytes - metabolism | Proteins | Drug resistance in microorganisms | Brain | Fluorescein | Physiological aspects | Glucose | Universities and colleges | Permeability | Dextrose | Endothelium
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9. Full Text VEGF Induces Tie2 Shedding via a Phosphoinositide 3-Kinase/Akt–Dependent Pathway to Modulate Tie2 Signaling
by Findley, Clarence M and Cudmore, Melissa J and Ahmed, Asif and Kontos, Christopher D
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 12/2007, Volume 27, Issue 12, pp. 2619 - 2626
OBJECTIVE—Tie2 and its ligands, the angiopoietins (Ang), are required for embryonic and postnatal angiogenesis. Previous studies have demonstrated that Tie2 is... 
Phosphoinositide 3-kinase | Akt | Tie2 | VEGF | Endothelium | endothelium | ACTIVATION | ANGIOGENESIS | TYROSINE KINASE | SOLUBLE TIE | GROWTH-FACTOR LEVELS | HUMAN ENDOTHELIAL-CELLS | OVEREXPRESSING ANGIOPOIETIN-1 | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | ANGIOPOIETIN RECEPTOR TIE-2 | EXPRESSION | phosphoinositide 3-kinase | PLASMA ANGIOPOIETIN-1 | NIH 3T3 Cells | Neovascularization, Physiologic - drug effects | Fibroblasts - enzymology | Phosphorylation | Tetradecanoylphorbol Acetate - pharmacology | Humans | Phosphatidylinositol 3-Kinases - metabolism | Vascular Endothelial Growth Factor A - metabolism | Angiopoietin-1 - metabolism | Phosphatidylinositol 3-Kinases - antagonists & inhibitors | Angiopoietin-2 - metabolism | Transfection | Receptor, TIE-2 - blood | Peptide Fragments - blood | Receptor, TIE-2 - metabolism | p38 Mitogen-Activated Protein Kinases - metabolism | Chromones - pharmacology | Proto-Oncogene Proteins c-akt - metabolism | Peptide Fragments - genetics | Fibroblasts - metabolism | Peptide Hydrolases - metabolism | PTEN Phosphohydrolase - genetics | Peptide Fragments - metabolism | Endothelial Cells - metabolism | Dipeptides - pharmacology | Cells, Cultured | Morpholines - pharmacology | PTEN Phosphohydrolase - metabolism | Imidazoles - pharmacology | Receptor, TIE-2 - genetics | Animals | Signal Transduction - drug effects | p38 Mitogen-Activated Protein Kinases - antagonists & inhibitors | Matrix Metalloproteinase Inhibitors | Mice | Protein Kinase Inhibitors - pharmacology | Pyridines - pharmacology | Matrix Metalloproteinases - metabolism | Endothelial Cells - pathology | Endothelial Cells - enzymology | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Apoptosis | Endothelial Cells - drug effects
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10. Full Text Endothelial progenitor cells give rise to pro-angiogenic smooth muscle-like progeny
by Moonen, Jan-Renier A. J and Krenning, Guido and Brinker, Marja G. L and Koerts, Jasper A and van Luyn, Marja J. A and Harmsen, Martin C
Cardiovascular Research, ISSN 0008-6363, 06/2010, Volume 86, Issue 3, pp. 506 - 515
Reciprocal plasticity exists between endothelial and mesenchymal lineages. For instance, mature endothelial cells adopt a smooth muscle-like phenotype through... 
Smooth muscle cells | EndMT | Transdifferentiation | Endothelial progenitor cells | Plasticity | INDUCED RECRUITMENT | CARDIAC & CARDIOVASCULAR SYSTEMS | TGF-BETA | VIVO | CORD BLOOD | PDGF-B | GROWTH-FACTOR-BETA | TO-MESENCHYMAL TRANSITION | IN-VITRO | EMBRYONIC STEM-CELLS | DIFFERENTIATION | Muscle, Smooth, Vascular - metabolism | Humans | Transforming Growth Factor beta1 - metabolism | Angiopoietin-1 - metabolism | Neoplasm Proteins - metabolism | Stem Cells - metabolism | Time Factors | Fibroblast Growth Factor 2 - metabolism | Cell Transdifferentiation | Myocytes, Smooth Muscle - metabolism | Protein-Serine-Threonine Kinases - metabolism | Biomarkers - metabolism | Paracrine Communication | Signal Transduction | Endothelial Cells - metabolism | Cells, Cultured | Smad2 Protein - metabolism | Vasoconstriction | Inhibitor of Differentiation Proteins - metabolism | Fetal Blood - cytology | Muscle, Smooth, Vascular - cytology | Cell Lineage | Phenotype | Receptors, Transforming Growth Factor beta - metabolism | Cytoskeleton - metabolism | Neovascularization, Physiologic
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11. 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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12. Full Text The ketogenic diet alters the hypoxic response and affects expression of proteins associated with angiogenesis, invasive potential and vascular permeability in a mouse glioma model
by Woolf, Eric C and Curley, Kara L and Liu, Qingwei and Turner, Gregory H and Charlton, Julie A and Preul, Mark C and Scheck, Adrienne C
PLoS ONE, ISSN 1932-6203, 06/2015, Volume 10, Issue 6, p. e0130357
Background The successful treatment of malignant gliomas remains a challenge despite the current standard of care, which consists of surgery, radiation and... 
SURVIVAL | ANTIANGIOGENIC THERAPY | GLIOBLASTOMA | HYPERGLYCEMIA | EDEMA | MULTIDISCIPLINARY SCIENCES | ENDOTHELIAL-CELLS | GROWTH | ANGIOPOIETIN-1 | PROMOTES | CANCER | Carbonic Anhydrases - genetics | Brain Neoplasms - pathology | Hypoxia - diet therapy | Cell Membrane Permeability | NF-kappa B - metabolism | Neovascularization, Pathologic - diet therapy | Brain Neoplasms - blood supply | Glioma - diet therapy | Vascular Endothelial Growth Factor A - metabolism | Vascular Endothelial Growth Factor A - genetics | Brain Neoplasms - metabolism | Immunoenzyme Techniques | Carbonic Anhydrases - metabolism | Glioma - metabolism | Hypoxia - metabolism | Neovascularization, Pathologic - pathology | Hypoxia-Inducible Factor 1, alpha Subunit - metabolism | Glioma - pathology | Aquaporin 4 - genetics | Biomarkers, Tumor - metabolism | Female | Zonula Occludens-1 Protein - metabolism | Real-Time Polymerase Chain Reaction | Carbonic Anhydrase IX | Disease Models, Animal | Brain Neoplasms - diet therapy | Zonula Occludens-1 Protein - genetics | Diet, Ketogenic | Hypoxia-Inducible Factor 1, alpha Subunit - genetics | Matrix Metalloproteinase 2 - metabolism | Neoplasm Invasiveness | Mice, Inbred C57BL | RNA, Messenger - genetics | Reverse Transcriptase Polymerase Chain Reaction | Glioma - blood supply | Matrix Metalloproteinase 2 - genetics | Animals | NF-kappa B - genetics | Hypoxia - pathology | Aquaporin 4 - metabolism | Biomarkers, Tumor - genetics | Mice | Neovascularization, Pathologic - metabolism | Low-carbohydrate diet | Aquaporins | Models | Permeability | Intermediate filament proteins | Health aspects | Vascular endothelial growth factor | Aquaporin 4 | Vimentin | Brain | Ketogenesis | Brain tumors | Brain cancer | Radiation | Oncology | Neurosurgery | Matrix metalloproteinase | Cancer therapies | High carbohydrate diet | High fat diet | Proteins | Angiogenesis | Low carbohydrate diet | Surgery | Life sciences | Metalloproteinase | Vascular endothelial growth factor receptor 2 | Growth factors | Research centers | Low protein diet | Edema | Carbohydrates | Phenotypes | Invasiveness | Metabolism | Survival | Brain research | Diet | Glioma | Carbonic anhydrase | Medical prognosis | Low fat diet | Hypoxia | Critical path | Microvasculature | Temozolomide | Laboratory animals | High protein diet | Tumors | Cancer
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13. 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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