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Journal of Cerebral Blood Flow & Metabolism, ISSN 0271-678X, 04/2007, Volume 27, Issue 4, pp. 697 - 709
Matrix metalloproteinases (MMPs) disrupt the blood—brain barrier (BBB) during reperfusion. Occludin and claudins are recently described tight junction proteins... 
Blood-brain barrier opening | Claudin-5 | Matrix metalloproteinases | Rat | Middle cerebral artery occlusion | Occludin | ACTIVATION | rat | PERMEABILITY | REPERFUSION | PROTEOLYSIS | BLOOD-BRAIN-BARRIER | NEUROSCIENCES | occludin | STRANDS | TYROSINE PHOSPHATASE INHIBITION | ENDOTHELIAL-CELLS | ENDOCRINOLOGY & METABOLISM | MATRIX-METALLOPROTEINASE-9 | HEMATOLOGY | matrix metalloproteinases | blood-brain barrier opening | middle cerebral artery occlusion | claudin-5 | Enzyme Activators - pharmacology | Immunohistochemistry | Cerebral Veins - metabolism | Sucrose | Brain Ischemia - metabolism | Male | Cerebral Arteries - drug effects | Protease Inhibitors - pharmacology | RNA, Messenger - biosynthesis | Gelatinases - metabolism | Membrane Proteins - metabolism | Matrix Metalloproteinases - biosynthesis | Tight Junctions - drug effects | Rats, Inbred SHR | Tight Junctions - metabolism | Astrocytes - drug effects | Furin - biosynthesis | Cerebral Veins - drug effects | Reperfusion Injury - pathology | Endothelial Cells - metabolism | Matrix Metalloproteinase 2 - metabolism | Rats | Infarction, Middle Cerebral Artery - pathology | Reverse Transcriptase Polymerase Chain Reaction | Blood-Brain Barrier - drug effects | Blotting, Western | Nerve Tissue Proteins - metabolism | Animals | Evans Blue | Cerebral Arteries - metabolism | Brain Ischemia - drug therapy | Matrix Metalloproteinase Inhibitors | Matrix Metalloproteinases - physiology | Astrocytes - metabolism | Endothelial Cells - drug effects
Journal Article
Circulation Research: Journal of the American Heart Association, ISSN 0009-7330, 06/2001, Volume 88, Issue 12, pp. 1276 - 1282
Itis generally accepted that endothelial cells generate most of their ATP byanaerobic glycolysis and that very little ATP is derived from the oxidation offatty... 
AICAR | Fuel metabolism | Acetyl CoA carboxylase | Glucose transport | Malonyl CoA | glucose transport | malonyl CoA | CARDIAC & CARDIOVASCULAR SYSTEMS | fuel metabolism | NITRIC-OXIDE SYNTHASE | OLEIC-ACID | ACETYL-COA CARBOXYLASE | VASCULAR ENDOTHELIUM | SKELETAL-MUSCLE | acetyl CoA carboxylase | METABOLISM | MALONYL-COA | GLUCOSE | PERIPHERAL VASCULAR DISEASE | NO SYNTHASE | HEMATOLOGY | CEREBRAL MICROVESSELS | Endothelium, Vascular - cytology | Palmitic Acid - metabolism | Humans | Multienzyme Complexes - metabolism | Endothelium, Vascular - drug effects | Tritium | Carnitine - metabolism | Caprylates - metabolism | Glycolysis - drug effects | AMP-Activated Protein Kinases | Aminoimidazole Carboxamide - pharmacology | Dose-Response Relationship, Drug | Ribonucleotides - pharmacology | Malonyl Coenzyme A - metabolism | Carnitine - pharmacology | Adenosine Triphosphate - metabolism | Oxidation-Reduction - drug effects | Aminoimidazole Carboxamide - metabolism | Energy Metabolism - physiology | Fatty Acids - metabolism | 3-O-Methylglucose - pharmacokinetics | Intracellular Fluid - metabolism | Protein-Serine-Threonine Kinases - metabolism | Ribonucleotides - metabolism | Cells, Cultured | Umbilical Veins | Glucose - pharmacology | Enzyme Activation - drug effects | Aminoimidazole Carboxamide - analogs & derivatives | Endothelium, Vascular - metabolism | Glucose - pharmacokinetics | Glucose - metabolism | Acetyl-CoA Carboxylase - metabolism | Energy Metabolism - drug effects
Journal Article
Lipids in Health and Disease, ISSN 1476-511X, 04/2017, Volume 16, Issue 1, pp. 77 - 10
Background: Atherosclerosis is a common cardiovascular disease that causes myocardial infarction, heart failure, and stroke. Increased oxidized low density... 
Oxidative stress | Oxidized low density lipoprotein | Human umbilical vein endothelial cells | Klotho | Lectin-like ox-LDL receptor | APOPTOSIS | ATHEROGENESIS | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | PROTECTS ENDOTHELIAL-CELLS | ATHEROSCLEROSIS | MECHANISMS | NUTRITION & DIETETICS | DISEASE | REQUIRES | DYSFUNCTION | SUPEROXIDE-DISMUTASE | Endothelium, Vascular - cytology | Reactive Oxygen Species - metabolism | Human Umbilical Vein Endothelial Cells - metabolism | Oxidative Stress | Phosphatidylinositol 3-Kinase - antagonists & inhibitors | Humans | Glucuronidase - metabolism | Superoxide Dismutase - antagonists & inhibitors | Proto-Oncogene Proteins c-akt - genetics | Reactive Oxygen Species - agonists | Nitric Oxide Synthase Type III - chemistry | Malondialdehyde - agonists | Human Umbilical Vein Endothelial Cells - cytology | Lipoproteins, LDL - metabolism | Nitric Oxide Synthase Type III - metabolism | Proto-Oncogene Proteins c-akt - metabolism | Phosphatidylinositol 3-Kinase - metabolism | Second Messenger Systems | Superoxide Dismutase - metabolism | Malondialdehyde - metabolism | Recombinant Proteins - metabolism | Atherosclerosis - pathology | Scavenger Receptors, Class E - agonists | Cell Survival | Nitric Oxide - antagonists & inhibitors | Cells, Cultured | Scavenger Receptors, Class E - antagonists & inhibitors | Nitric Oxide Synthase Type III - genetics | Atherosclerosis - metabolism | Nitric Oxide - agonists | Phosphatidylinositol 3-Kinase - chemistry | Superoxide Dismutase - chemistry | Scavenger Receptors, Class E - metabolism | Reactive Oxygen Species - antagonists & inhibitors | Human Umbilical Vein Endothelial Cells - enzymology | Glucuronidase - genetics | Lipoproteins, LDL - antagonists & inhibitors | Phosphatidylinositol 3-Kinase - genetics | Endothelium, Vascular - metabolism | Proto-Oncogene Proteins c-akt - agonists | Endothelium, Vascular - pathology | Lipid Peroxidation | Malondialdehyde - antagonists & inhibitors | Nitric Oxide - metabolism | Proto-Oncogene Proteins c-akt - antagonists & inhibitors | Myocardial infarction | Lipoproteins (low density) | Atherogenesis | Superoxide dismutase | Cardiovascular disease | AKT protein | Cell adhesion & migration | Proteins | Lysates | Cell growth | Atherosclerosis | Aging | Tumor necrosis factor-TNF | Heart diseases | Cerebral infarction | Stroke | Inositol | Cytokines | LOX-1 protein | Low density lipoprotein | Nitric-oxide synthase | Malondialdehyde | Endothelial cells | 1-Phosphatidylinositol 3-kinase | Endothelium | Polymerase chain reaction | Klotho protein | Arteriosclerosis | Nitric oxide | Calcification | Diabetes | Umbilical vein | Apoptosis
Journal Article
Developmental Cell, ISSN 1534-5807, 09/2017, Volume 42, Issue 5, pp. 445 - 461.e5
Journal Article
PLoS ONE, ISSN 1932-6203, 06/2018, Volume 13, Issue 6, p. e0198617
Journal Article
Circulation Research, ISSN 0009-7330, 03/2010, Volume 106, Issue 4, pp. 739 - 747
Journal Article
Brain, ISSN 0006-8950, 12/2009, Volume 132, Issue 12, pp. 3231 - 3241
A role for the Notch signalling pathway in the formation of arteriovenous malformations during development has been suggested. However, whether Notch... 
Human | AVM | Angiogenesis | Brain | Signalling | Notch-1 | DEFECTS | angiogenesis | brain | CELL FATE | NEUROSCIENCES | CLINICAL NEUROLOGY | ARTERIAL | LETHALITY | PATHWAY | EMBRYONIC VASCULAR DEVELOPMENT | MICE | JAGGED1 | MUTATIONS | human | EXPRESSION | signalling | Role | Neurological Impairments | Cognitive Processes | Animals | Surgery | Neurological Organization | Cytology | Genetics | Control Groups | Immunohistochemistry | Transcription Factor HES-1 | Cerebral Veins - metabolism | Muscle, Smooth, Vascular - metabolism | Homeodomain Proteins - metabolism | Humans | Middle Aged | Male | Intracranial Arteriovenous Malformations - physiopathology | Muscle, Smooth, Vascular - physiopathology | Intracranial Arteriovenous Malformations - metabolism | Young Adult | Intercellular Signaling Peptides and Proteins - metabolism | Basic Helix-Loop-Helix Transcription Factors - metabolism | Serrate-Jagged Proteins | Adult | Female | Neovascularization, Pathologic - physiopathology | Membrane Proteins - metabolism | Child | Jagged-1 Protein | Calcium-Binding Proteins - metabolism | Endothelial Cells - metabolism | Cerebral Arteries - physiopathology | Neovascularization, Pathologic - chemically induced | Receptor, Notch1 - metabolism | Intracranial Arteriovenous Malformations - pathology | Muscle, Smooth, Vascular - pathology | Cerebral Veins - physiopathology | Signal Transduction - drug effects | Cerebral Arteries - metabolism | Adolescent | Cerebral Arteries - pathology | Signal Transduction - physiology | Aged | Neovascularization, Pathologic - metabolism | Cerebral Veins - pathology | Endothelial Cells - pathology | Original
Journal Article
Vascular Pharmacology, ISSN 1537-1891, 2015, Volume 73, pp. 149 - 157
Abstract Hypoxia/reoxygenation (H/R) induces endothelial inflammation with augmentation of endothelial adhesion molecules over-expression. Propofol was... 
Cardiovascular | Endothelial | Hypoxia/reoxygenation | Propofol | OXIDATIVE STRESS | ICAM-1 EXPRESSION | INJURY | PROTECTS | OXIDE SYNTHASE PHOSPHORYLATION | CEREBRAL ISCHEMIA-REPERFUSION | LEUKOCYTE ADHESION MOLECULES | NITRIC-OXIDE | MITOCHONDRIAL DYSFUNCTION | PHARMACOLOGY & PHARMACY | NF-KAPPA-B | Enzyme Activators - pharmacology | Inflammation - pathology | Phosphorylation | Shc Signaling Adaptor Proteins - metabolism | Humans | Propofol - pharmacology | NF-kappa B - metabolism | Dose-Response Relationship, Drug | Inflammation Mediators - metabolism | Superoxides - metabolism | Peptidylprolyl Isomerase - metabolism | Nitric Oxide Synthase Type III - metabolism | Human Umbilical Vein Endothelial Cells - drug effects | Protein Phosphatase 2 - antagonists & inhibitors | Reperfusion Injury - pathology | Anti-Inflammatory Agents - pharmacology | Reperfusion Injury - enzymology | Down-Regulation | Cells, Cultured | Enzyme Inhibitors - pharmacology | NIMA-Interacting Peptidylprolyl Isomerase | Cell Adhesion - drug effects | Cell Adhesion Molecules - metabolism | Protein Transport | Human Umbilical Vein Endothelial Cells - enzymology | Reperfusion Injury - prevention & control | Src Homology 2 Domain-Containing, Transforming Protein 1 | Signal Transduction - drug effects | Protein Phosphatase 2 - metabolism | Human Umbilical Vein Endothelial Cells - pathology | Inflammation - prevention & control | Nitric Oxide - metabolism | Inflammation - enzymology | Phenols | Inflammation | Phosphatases | Nitric oxide | Endothelium
Journal Article
PLoS ONE, ISSN 1932-6203, 11/2012, Volume 7, Issue 11, p. e49701
Paeoniflorin (PF), the principal component of Paeoniae Radix prescribed in traditional Chinese medicine, has been reported to exhibit many pharmacological... 
STROKE | ACTIVATION | PATHWAY | NEUROVASCULAR UNIT | MULTIDISCIPLINARY SCIENCES | FOCAL CEREBRAL-ISCHEMIA | INTRACEREBRAL HEMORRHAGE | NITRIC-OXIDE | MECHANISMS | EXPRESSION | NEUROPROTECTION | Microglia - metabolism | Tumor Necrosis Factor-alpha - blood | Tumor Necrosis Factor-alpha - genetics | Male | NF-kappa B - metabolism | Interleukin-1beta - genetics | Brain - metabolism | Inflammation - metabolism | Bridged-Ring Compounds - pharmacology | Monoterpenes | Neurons - metabolism | Disease Models, Animal | NF-kappa B - antagonists & inhibitors | bcl-2-Associated X Protein - metabolism | Rats | Brain - drug effects | Signal Transduction - drug effects | Brain Ischemia - drug therapy | Benzoates - pharmacology | Brain - pathology | Bridged-Ring Compounds - administration & dosage | Astrocytes - metabolism | Nitric Oxide Synthase Type II - metabolism | Cerebral Infarction - drug therapy | Brain Ischemia - metabolism | Cytochromes c - genetics | Hippocampus - drug effects | Anti-Inflammatory Agents, Non-Steroidal - pharmacology | Interleukin-1beta - blood | Proto-Oncogene Proteins c-bcl-2 - metabolism | Lipoxygenase - metabolism | Cerebral Infarction - metabolism | Inflammation - drug therapy | Neurons - drug effects | bcl-2-Associated X Protein - genetics | Cerebral Infarction - pathology | Astrocytes - drug effects | Glucosides - pharmacology | Microglia - drug effects | Cytochromes c - metabolism | Benzoates - administration & dosage | Gene Expression Regulation - drug effects | Animals | Glucosides - administration & dosage | Mitogen-Activated Protein Kinases - antagonists & inhibitors | Anti-Inflammatory Agents, Non-Steroidal - administration & dosage | Cyclooxygenase 2 - metabolism | Proto-Oncogene Proteins c-bcl-2 - genetics | Mitogen-Activated Protein Kinases - metabolism | Occlusion | Neuroprotection | Brain | Inflammatory response | Activation | Kinases | Carotid arteries | Signal transduction | Chinese medicine | Ischemia | Neurodegeneration | Cerebral blood flow | Rodents | Tumor necrosis factor-TNF | Inhibition | NF-κB protein | Stroke | Cytokines | Astrocytes | Traditional Chinese medicine | Extracellular signal-regulated kinase | MAP kinase | JNK protein | Pharmacology | Inflammation | Tumor necrosis factor-α | IL-1β | Nitric-oxide synthase | Microglia | Signaling | Brain research | Liquid oxygen | Hypoxia | Brain damage | Cyclooxygenase-2 | Laboratory animals | Apoptosis | Veins & arteries
Journal Article
Journal of Molecular Neuroscience, ISSN 0895-8696, 2/2014, Volume 52, Issue 2, pp. 261 - 268
Atherosclerotic cerebral infarction (ACI) is characterized by extremely high fatality and disability rate. Recent studies indicate that co-stimulatory signal... 
Neurochemistry | Neurology | Atherosclerotic cerebral infarction | Neurosciences | Biomedicine | OX40L | Proteomics | Rosuvastatin | hs-CRP | PPAR-γ | Cell Biology | ACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | LOW-DENSITY-LIPOPROTEIN | CD4(+) T-CELLS | SUPPRESSION | NEUROSCIENCES | LESIONS |