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1. Full Text Sulforaphane preconditioning of the Nrf2/HO-1 defense pathway protects the cerebral vasculature against blood–brain barrier disruption and neurological deficits in stroke
by Alfieri, Alessio and Srivastava, Salil and Siow, Richard C.M and Cash, Diana and Modo, Michel and Duchen, Michael R and Fraser, Paul A and Williams, Steven C.R and Mann, Giovanni E
Free Radical Biology and Medicine, ISSN 0891-5849, 12/2013, Volume 65, pp. 1012 - 1022
Disruption of the blood–brain barrier (BBB) and cerebral edema are the major pathogenic mechanisms leading to neurological dysfunction and death after ischemic... 
Stroke | Nrf2 | Sulforaphane | Heme oxygenase | Gliovascular complex | Preconditioning | Blood–brain barrier | Blood-brain barrier | OXIDATIVE STRESS | ISCHEMIC BRAIN | ARTERY OCCLUSION | BIOCHEMISTRY & MOLECULAR BIOLOGY | Hems oxygenase | HEME OXYGENASE-1 GENE | BEHAVIORAL-ASSESSMENT | PERMEABILITY TRANSITION | TRANSCRIPTION FACTOR NRF2 | ENDOCRINOLOGY & METABOLISM | RAT-BRAIN | NEUROVASCULAR PROTECTION | MOLECULAR-MECHANISMS | Neuroprotective Agents - therapeutic use | Up-Regulation | Heme Oxygenase-1 - metabolism | Oxidative Stress | Male | Infarction, Middle Cerebral Artery - metabolism | Cerebral Arteries - drug effects | Heme Oxygenase-1 - genetics | Psychomotor Disorders - metabolism | Isothiocyanates - therapeutic use | Neuroprotective Agents - pharmacology | NF-E2-Related Factor 2 - genetics | Infarction, Middle Cerebral Artery - drug therapy | Membrane Proteins - metabolism | Microvessels - enzymology | Psychomotor Disorders - prevention & control | Reperfusion Injury - metabolism | Isothiocyanates - pharmacology | Gene Expression | Signal Transduction | Membrane Proteins - genetics | Blood-Brain Barrier - drug effects | Rats, Sprague-Dawley | Blood-Brain Barrier - metabolism | Blood-Brain Barrier - pathology | Animals | Reperfusion Injury - prevention & control | Cerebral Arteries - enzymology | NF-E2-Related Factor 2 - metabolism | Stroke (Disease) | Antioxidants | Analysis | Antigens | Brain | Heme | Injuries | Index Medicus
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2. Full Text Oxidative stress activates protein tyrosine kinase and matrix metalloproteinases leading to blood–brain barrier dysfunction
by Haorah, James and Ramirez, Servio H and Schall, Kathy and Smith, Daniel and Pandya, Rita and Persidsky, Yuri
Journal of Neurochemistry, ISSN 0022-3042, 04/2007, Volume 101, Issue 2, pp. 566 - 576
The blood–brain barrier (BBB) formed by brain microvascular endothelial cells (BMVEC) regulates the passage of molecules and leukocytes in and out of the... 
blood–brain barrier | protein tyrosine kinase | matrix metalloproteinases | protein tyrosine phosphatase | brain endothelial cell | oxidative stress | Protein tyrosine kinase | Oxidative stress | Matrix metalloproteinases | Blood-brain barrier | Brain endothelial cell | Protein tyrosine phosphatase | blood-brain barrier | HUMAN STROKE | FACTOR RECEPTOR TRANSACTIVATION | BIOCHEMISTRY & MOLECULAR BIOLOGY | FOCAL CEREBRAL-ISCHEMIA | VASCULAR-PERMEABILITY | TIGHT JUNCTION | NEUROSCIENCES | SIGNAL-TRANSDUCTION | MULTIPLE-SCLEROSIS | ENDOTHELIAL-CELLS | RHO GTPASES | EXTRACELLULAR-MATRIX | Reactive Oxygen Species - metabolism | Protein-Tyrosine Kinases - metabolism | Humans | Oxidative Stress - physiology | Reactive Oxygen Species - pharmacology | Blood-Brain Barrier - physiopathology | Basement Membrane - pathology | Chemotaxis, Leukocyte - physiology | Tissue Inhibitor of Metalloproteinase-1 - metabolism | Encephalitis - physiopathology | Chemotaxis, Leukocyte - drug effects | Up-Regulation - physiology | Basement Membrane - enzymology | Tight Junctions - metabolism | Encephalitis - enzymology | Cells, Cultured | Enzyme Inhibitors - pharmacology | Cerebral Arteries - physiopathology | Basement Membrane - metabolism | Blood-Brain Barrier - enzymology | Neurodegenerative Diseases - physiopathology | Cerebral Arteries - enzymology | Endothelial Cells - cytology | Matrix Metalloproteinases - metabolism | Endothelial Cells - enzymology | Enzyme Activation - physiology | Neurodegenerative Diseases - enzymology | Neurosciences | Biochemistry | Oxidation | Brain research | Kinases | Neurological disorders | Index Medicus
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3. Full Text Association of Low Lysosomal Enzymes Activity With Brain Arterial Dilatation
by Shah, Harsh and Shah, Harsh and Liong, Christopher and Liong, Christopher and Levy, Oren A and Levy, Oren A and Waters, Cheryl and Waters, Cheryl and Fahn, Stanley and Fahn, Stanley and Marder, Karen and Marder, Karen and Kang, Un J and Kang, Un J and Wolf, Pavlina and Wolf, Pavlina and Oliva, Petra and Oliva, Petra and Zhang, Kate and Zhang, Kate and Alcalay, Roy N and Alcalay, Roy N and Gutierrez, Jose and Gutierrez, Jose
Stroke, ISSN 0039-2499, 2018, Volume 49, Issue 8, pp. 1977 - 1980
Background and Purpose- Absent or diminished α-galactosidase A (GLA) and acid α-glucosidase (GAA) enzyme activity are core features of Fabry and Pompe disease,... 
lysosomes | inflammation | sphingolipids | hypertension | dilatation | Brain - diagnostic imaging | Cerebral Arteries - diagnostic imaging | Humans | Middle Aged | Dilatation, Pathologic - enzymology | Brain - enzymology | Lysosomes - enzymology | Male | Parkinsonian Disorders - enzymology | alpha-Galactosidase - metabolism | Brain - blood supply | Cerebral Arteries - enzymology | Parkinsonian Disorders - diagnostic imaging | Glucan 1,4-alpha-Glucosidase - metabolism | Female | Aged | Enzyme Activation - physiology | Cohort Studies
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4. Full Text Catalpol stimulates VEGF production via the JAK2/STAT3 pathway to improve angiogenesis in rats’ stroke model
by Dong, Wan and Xian, Yang and Yuan, Wang and Huifeng, Zhu and Tao, Wang and Zhiqiang, Liu and Shan, Feng and Ya, Fu and Hongli, Wang and Jinghuan, Wang and Lei, Qin and Li, Zou and Hongyi, Qi
Journal of Ethnopharmacology, ISSN 0378-8741, 09/2016, Volume 191, pp. 169 - 179
Catalpol is the main active component of the radix from Libosch, which has pleiotropic protective effects in neurodegenerative diseases, ischemic stroke,... 
Angiogenesis | JAK2/STAT3 | Catalpol | VEGF | TYROSINE-PHOSPHATASE SHP-1 | CHEMISTRY, MEDICINAL | ARTERY OCCLUSION | FOCAL CEREBRAL-ISCHEMIA | REPERFUSION INJURY | PLANT SCIENCES | STAT3 ACTIVATION | PLASMINOGEN-ACTIVATOR | SIGNALING PATHWAY | INTEGRATIVE & COMPLEMENTARY MEDICINE | ERYTHROPOIETIN PROMOTES | PHARMACOLOGY & PHARMACY | CENTRAL-NERVOUS-SYSTEM | ENDOTHELIAL GROWTH-FACTOR | Infarction, Middle Cerebral Artery - physiopathology | Iridoid Glucosides - pharmacology | Neovascularization, Physiologic - drug effects | Up-Regulation | Phosphorylation | Transcriptional Activation | Brain - enzymology | Male | Vascular Endothelial Growth Factor A - metabolism | RNA, Messenger - metabolism | Vascular Endothelial Growth Factor A - genetics | Cerebral Arteries - drug effects | Neuroprotective Agents - pharmacology | Time Factors | Janus Kinase 2 - metabolism | Infarction, Middle Cerebral Artery - drug therapy | Angiogenesis Inducing Agents - pharmacology | Erythropoietin - metabolism | STAT3 Transcription Factor - metabolism | Disease Models, Animal | Promoter Regions, Genetic | Cerebrovascular Circulation - drug effects | Brain - physiopathology | RNA, Messenger - genetics | Cerebral Arteries - physiopathology | Infarction, Middle Cerebral Artery - pathology | Rats, Sprague-Dawley | Brain - drug effects | Animals | Signal Transduction - drug effects | Cerebral Arteries - enzymology | Cerebral Arteries - pathology | Brain - pathology | Protein Binding | Infarction, Middle Cerebral Artery - enzymology | Receptors, Erythropoietin - metabolism | Stroke (Disease) | Drugstores | Nervous system diseases | Medicine, Chinese | Endothelial growth factors | Pharmacy | Brain | Yuan (China) | Injuries | Index Medicus
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5. Full Text Pharmacological Inhibition of Phospholipase D Protects Mice From Occlusive Thrombus Formation and Ischemic Stroke—Brief Report
by Stegner, David and Thielmann, Ina and Kraft, Peter and Frohman, Michael A and Stoll, Guido and Nieswandt, Bernhard
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 09/2013, Volume 33, Issue 9, pp. 2212 - 2217
OBJECTIVE—We recently showed that mice lacking the lipid signaling enzyme phospholipase (PL) D1 or both PLD isoforms (PLD1 and PLD2) were protected from... 
phospholipase D | thrombosis | 5-fluoro-2-indolyl des-chlorohalopemide | cerebral stroke | PLATELETS | RISK | PERIPHERAL VASCULAR DISEASE | HEMATOLOGY | MOLECULAR-MECHANISMS | HALOPEMIDE | Carotid Artery Diseases - prevention & control | Infarction, Middle Cerebral Artery - physiopathology | Infarction, Middle Cerebral Artery - prevention & control | Carotid Artery Diseases - physiopathology | Blood Platelets - enzymology | Recovery of Function | Dose-Response Relationship, Drug | Time Factors | Infarction, Middle Cerebral Artery - genetics | Indoles - pharmacology | Phospholipase D - genetics | Thrombosis - blood | Thrombosis - prevention & control | Blood Platelets - drug effects | Domperidone - analogs & derivatives | Integrins - blood | Disease Models, Animal | Hemostasis - drug effects | Thrombosis - physiopathology | Phospholipase D - deficiency | Mice, Inbred C57BL | Thrombosis - enzymology | Enzyme Inhibitors - pharmacology | Phospholipase D - antagonists & inhibitors | Infarction, Middle Cerebral Artery - blood | Mice, Knockout | Fibrinolytic Agents - pharmacology | Animals | Carotid Artery Diseases - enzymology | Carotid Artery Diseases - blood | Carotid Artery Diseases - genetics | Domperidone - pharmacology | Thrombosis - genetics | Mice | Infarction, Middle Cerebral Artery - enzymology | Index Medicus
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6. Full Text NADPH Oxidase Activity and Function Are Profoundly Greater in Cerebral Versus Systemic Arteries
by Miller, Alyson A and Drummond, Grant R and Schmidt, Harald H.H.W and Sobey, Christopher G
Circulation Research, ISSN 0009-7330, 11/2005, Volume 97, Issue 10, pp. 1055 - 1062
Recent studies suggest that the superoxide generating enzyme NADPH oxidase may play a functional role in regulating cerebral vascular tone. We tested whether... 
Reactive oxygen species | Cerebral | Hydrogen peroxide | Angiotensin II | NADPH oxidase | CARDIAC & CARDIOVASCULAR SYSTEMS | SUPEROXIDE-PRODUCTION | MAJOR SOURCE | hydrogen peroxide | MECHANISMS | VASCULAR SMOOTH-MUSCLE | ARACHIDONATE | TONE | angiotensin II | reactive oxygen species | ENDOTHELIAL-CELLS | PERIPHERAL VASCULAR DISEASE | VASODILATATION | HYPERTENSION | STRESS | HEMATOLOGY | cerebral | Angiotensin II - pharmacology | Reactive Oxygen Species - metabolism | Hydrogen Peroxide - pharmacology | RNA, Messenger - analysis | Rats | Male | NADPH Oxidases - blood | NADPH Oxidase 4 | Nitroprusside - pharmacology | Rats, Sprague-Dawley | Vasoconstriction - drug effects | NADP - pharmacology | Animals | Arteries - enzymology | Cerebral Arteries - enzymology | Superoxides - metabolism | NADPH Oxidases - genetics | Vasodilation - drug effects | NADPH Oxidases - physiology | Index Medicus
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7. Full Text Cigarette Smoke Initiates Oxidative Stress-Induced Cellular Phenotypic Modulation Leading to Cerebral Aneurysm Pathogenesis
by Starke, Robert M and Thompson, John W and Ali, Muhammad S and Pascale, Crissey L and Martinez Lege, Alejandra and Ding, Dale and Chalouhi, Nohra and Hasan, David M and Jabbour, Pascal and Owens, Gary K and Toborek, Michal and Hare, Joshua M and Dumont, Aaron S
Arteriosclerosis, Thrombosis, and Vascular Biology, ISSN 1079-5642, 03/2018, Volume 38, Issue 3, pp. 610 - 621
OBJECTIVE—Cigarette smoke exposure (CSE) is a risk factor for cerebral aneurysm (CA) formation, but the molecular mechanisms are unclear. Although CSE is known... 
Oxygen | Smoke | Subarachnoid hemorrhage | Aneurysm | Atherosclerosis | Rupture | atherosclerosis | aneurysm | RISK-FACTORS | smoke | NATURAL-HISTORY | rupture | subarachnoid hemorrhage | IN-VIVO | UNRUPTURED INTRACRANIAL ANEURYSMS | CARDIOVASCULAR-DISEASE | PERIPHERAL VASCULAR DISEASE | SMOOTH-MUSCLE-CELLS | CORONARY-HEART-DISEASE | HEMATOLOGY | oxygen | ISCHEMIC-STROKE | MOLECULAR-MECHANISMS | Vascular Remodeling | Oxidative Stress | Myocytes, Smooth Muscle - pathology | NADPH Oxidases - metabolism | Aneurysm, Ruptured - prevention & control | Male | Intracranial Aneurysm - prevention & control | Acetophenones - pharmacology | NADPH Oxidases - genetics | Intracranial Aneurysm - enzymology | Dilatation, Pathologic | Disease Models, Animal | Cigarette Smoking - adverse effects | Signal Transduction | Intracranial Aneurysm - genetics | Myocytes, Smooth Muscle - enzymology | NADPH Oxidases - antagonists & inhibitors | Cells, Cultured | NADPH Oxidase 1 - genetics | Antioxidants - pharmacology | Rats, Sprague-Dawley | Mice, Knockout | Muscle, Smooth, Vascular - pathology | Phenotype | Aneurysm, Ruptured - enzymology | Animals | Cerebral Arteries - enzymology | Cerebral Arteries - pathology | NADPH Oxidase 1 - metabolism | Aneurysm, Ruptured - pathology | Intracranial Aneurysm - pathology | Aneurysm, Ruptured - genetics | Muscle, Smooth, Vascular - enzymology | Index Medicus | Hypertension | stress | cigarette | Vascular Biology | cerebrovascular | Smooth muscle | Inflammation | phenotypic modulation | Cerebral Aneurysms | stroke | reactive | species | Ischemic Stroke | oxidative | Cerebrovascular Disease | Intracranial Hemorrhage
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8. Full Text Testosterone Alters Maternal Vascular Adaptations: Role of the Endothelial NO System
by Chinnathambi, Vijayakumar and Balakrishnan, Meena and Ramadoss, Jayanth and Yallampalli, Chandrasekhar and Sathishkumar, Kunju
Hypertension, ISSN 0194-911X, 03/2013, Volume 61, Issue 3, pp. 647 - 654
Sex steroid hormones estradiol and progesterone play an important role in vascular adaptations during pregnancy. However, little is known about the role of... 
blood pressure | eNOS phosphorylation | prostacyclin | vasodilation | mesenteric arteries | hypertension | endothelium-derived hyperpolarizing factor | NITRIC-OXIDE SYNTHESIS | ANGIOTENSIN-II | MESENTERIC-ARTERY | UTERINE ARTERY | BLOOD-PRESSURE | PERIPHERAL VASCULAR DISEASE | ANDROGEN LEVELS | CEREBRAL-ARTERIES | GROWTH RESTRICTION | RENAL INJURY | VASODILATOR PRODUCTION | Mesenteric Arteries - physiology | Phosphorylation | Adaptation, Physiological - drug effects | Testosterone - physiology | Nitric Oxide Synthase Type III - analysis | Endothelium, Vascular - drug effects | Mesenteric Arteries - drug effects | Nitroprusside - pharmacology | Endothelium, Vascular - enzymology | Testosterone - pharmacology | Threonine - metabolism | Hypertension, Pregnancy-Induced - drug therapy | Endothelium, Vascular - physiology | Arterial Pressure | Epoprostenol - pharmacology | Female | Nitric Oxide Synthase Type III - metabolism | Testosterone - blood | Hypertension, Pregnancy-Induced - enzymology | Vasodilator Agents - pharmacology | Acetylcholine - pharmacology | Adaptation, Physiological - physiology | Rats | Hypertension, Pregnancy-Induced - physiopathology | Nitric Oxide - physiology | Rats, Sprague-Dawley | Serine - metabolism | Nitric Oxide Synthase Type III - antagonists & inhibitors | Pregnancy | Animals | Mesenteric Arteries - enzymology | Biological Factors - pharmacology | Index Medicus
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9. Full Text Macrophage-derived matrix metalloproteinase-2 and -9 promote the progression of cerebral aneurysms in rats
by Aoki, Tomohiro and Kataoka, Hiroharu and Morimoto, Masafumi and Nozaki, Kazuhiko and Hashimoto, Nobuo
Stroke, ISSN 0039-2499, 01/2007, Volume 38, Issue 1, pp. 162 - 169
Background and Purpose-Mechanisms of initiation, progression and rupture of cerebral aneurysms have not yet been fully understood despite its clinical... 
Inflammation | Matrix metalloproteinases | Macrophages | Aneurysm | aneurysm | macrophages | GELATINASE | DISRUPTION | ABDOMINAL AORTIC-ANEURYSMS | inflammation | RUPTURE | PERIPHERAL VASCULAR DISEASE | HYPERTENSION | matrix metalloproteinases | EXPERIMENTAL INDUCTION | CLINICAL NEUROLOGY | Immunohistochemistry | Vasculitis - physiopathology | Male | Chemotaxis, Leukocyte - physiology | Macrophages - secretion | Matrix Metalloproteinase 9 - metabolism | Chemotaxis, Leukocyte - drug effects | Matrix Metalloproteinase 9 - secretion | Intracranial Aneurysm - enzymology | Disease Models, Animal | Matrix Metalloproteinase 2 - metabolism | Enzyme Inhibitors - pharmacology | Rats | Cerebral Arteries - physiopathology | Reverse Transcriptase Polymerase Chain Reaction | Rats, Sprague-Dawley | Disease Progression | Macrophages - enzymology | Animals | Cerebral Arteries - enzymology | Matrix Metalloproteinase Inhibitors | Vasculitis - enzymology | Macrophages - drug effects | Matrix Metalloproteinase 2 - secretion | Intracranial Aneurysm - physiopathology | Index Medicus
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10. Full Text NADPH-oxidase activity is elevated in penumbral and non-ischemic cerebral arteries following stroke
by Miller, Alyson A and Dusting, Gregory J and Roulston, Carli L and Sobey, Christopher G
Brain Research, ISSN 0006-8993, 2006, Volume 1111, Issue 1, pp. 111 - 116
Reactive oxygen species play a role in neuronal damage following cerebral ischemia–reperfusion. We tested whether activity of the superoxide-generating enzyme,... 
Oxidative stress | Cerebral vasculature | Stroke | Cerebral ischemia | NADPH-oxidase | SUPEROXIDE | MICROGLIAL CELLS | BLOOD-FLOW | stroke | NEUROSCIENCES | cerebral vasculature | VASCULAR SMOOTH-MUSCLE | SENSORIMOTOR DEFICITS | NEURONAL DAMAGE | CONSCIOUS RATS | NEUROPROTECTIVE AGENT | cerebral ischemia | IN-VIVO | ISCHEMIC-STROKE | oxidative stress | Infarction, Middle Cerebral Artery - physiopathology | Reactive Oxygen Species - metabolism | Cerebral Cortex - blood supply | Cerebrovascular Circulation - physiology | Rats, Wistar | NADPH Oxidases - metabolism | Male | Stroke - physiopathology | Cerebral Cortex - physiopathology | Brain Ischemia - enzymology | Basilar Artery - physiopathology | Time Factors | Up-Regulation - physiology | Middle Cerebral Artery - physiopathology | Superoxides - metabolism | Functional Laterality - physiology | Disease Models, Animal | Basilar Artery - enzymology | Cerebral Cortex - enzymology | Reperfusion Injury - enzymology | NADPH Oxidases - antagonists & inhibitors | Enzyme Inhibitors - pharmacology | Rats | Cerebral Arteries - physiopathology | Brain Ischemia - physiopathology | Onium Compounds - pharmacology | Stroke - enzymology | Middle Cerebral Artery - enzymology | Animals | Cerebral Arteries - enzymology | Reperfusion Injury - physiopathology | Infarction, Middle Cerebral Artery - enzymology | Stroke (Disease) | Enzymes | Oxides | Hydrogen peroxide | Analysis | Arteries | Index Medicus
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11. Full Text Rutin protects the neural damage induced by transient focal ischemia in rats
by Khan, Mohd. Moshahid and Ahmad, Ajmal and Ishrat, Tauheed and Khuwaja, Gulrana and Srivastawa, Pallavi and Khan, M. Badruzzaman and Raza, Syed Shadab and Javed, Hayate and Vaibhav, Kumar and Khan, Andleeb and Islam, Fakhrul
Brain Research, ISSN 0006-8993, 2009, Volume 1292, pp. 123 - 135
Abstract Free radical induced neural damage is implicated in cerebral ischemia–reperfusion (IR) injury and antioxidants are reported to have neuroprotective... 
Neurology | Oxidative stress | Neurobehavior | Ischemia | Rutin | Brain infarct | Apoptosis | MIDDLE CEREBRAL-ARTERY | LIPID-PEROXIDATION | INJURY | NEUROCHEMICAL CHANGES | NEUROSCIENCES | FREE-RADICALS | CELL-DEATH | ANTIOXIDANT STATUS | SPATIAL MEMORY IMPAIRMENT | MOLECULAR-MECHANISMS | Neurons - pathology | Rats, Wistar | Glutathione - metabolism | Antioxidants - metabolism | Rutin - pharmacology | Brain - enzymology | Motor Activity - drug effects | Male | Hippocampus - drug effects | Neuroprotective Agents - pharmacology | Time Factors | Cell Death | Hippocampus - enzymology | Infarction, Middle Cerebral Artery - drug therapy | Neurons - drug effects | Neuroprotective Agents - administration & dosage | Tumor Suppressor Protein p53 - metabolism | Rats | Thiobarbituric Acid Reactive Substances - metabolism | Hippocampus - pathology | Infarction, Middle Cerebral Artery - pathology | Frontal Lobe - enzymology | Hydrogen Peroxide - metabolism | Brain - drug effects | Animals | Frontal Lobe - drug effects | Neurons - enzymology | Rutin - administration & dosage | Brain - pathology | Infarction, Middle Cerebral Artery - enzymology | Frontal Lobe - pathology | Antioxidants | Neurons | Glycosides | Superoxide dismutase | Superoxide | Tumor proteins | Glutathione | Index Medicus
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12. Full Text Activated Protein C Promotes Neovascularization and Neurogenesis in Postischemic Brain via Protease-Activated Receptor 1
by Thiyagarajan, Meenakshisundaram and Fernandez, Jose A and Lane, Steven M and Griffin, John H and Zlokovic, Berislav V
Journal of Neuroscience, ISSN 0270-6474, 11/2008, Volume 28, Issue 48, pp. 12788 - 12797
Activated protein C (APC) is a serine protease with anticoagulant and direct cytoprotective activities. Early postischemic APC application activates the... 
Angiogenesis | Neuroprotection | Serine protease | Activated protein C | Neurogenesis | Transient cerebral ischemia | FUNCTIONAL RECOVERY | ARTERY OCCLUSION | angiogenesis | FOCAL CEREBRAL-ISCHEMIA | CELL-PROLIFERATION | SUBVENTRICULAR ZONE | serine protease | NEUROSCIENCES | NEURONAL DAMAGE | transient cerebral ischemia | TISSUE-PLASMINOGEN-ACTIVATOR | neuroprotection | IN-VIVO | neurogenesis | EMBOLIC STROKE | activated protein C | SEVERE SEPSIS | Neovascularization, Physiologic - drug effects | Recovery of Function - drug effects | Nerve Regeneration - physiology | Blood-Brain Barrier - physiopathology | Brain - enzymology | Male | Cell Movement - physiology | Protein C - pharmacology | Brain - metabolism | Brain Ischemia - enzymology | Recovery of Function - physiology | Neurogenesis - drug effects | Tissue Plasminogen Activator - toxicity | Brain Infarction - drug therapy | Disease Models, Animal | Brain Infarction - enzymology | Reperfusion Injury - enzymology | Brain - physiopathology | Mice, Inbred C57BL | Cerebral Arteries - physiopathology | Treatment Outcome | Brain Ischemia - physiopathology | Brain Infarction - physiopathology | Blood-Brain Barrier - drug effects | Receptor, PAR-1 - genetics | Blood-Brain Barrier - metabolism | Mice, Knockout | Cell Movement - drug effects | Neovascularization, Physiologic - physiology | Animals | Cerebral Arteries - enzymology | Cerebral Arteries - metabolism | Neurogenesis - physiology | Brain Ischemia - drug therapy | Reperfusion Injury - physiopathology | Cell Proliferation - drug effects | Mice | Protein C - metabolism | Enzyme Activation - physiology | Index Medicus
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13. Full Text NEU1 and NEU3 sialidase activity expressed in human lung microvascular endothelia: NEU1 restrains endothelial cell migration, whereas NEU3 does not
by Cross, Alan S and Hyun, Sang Won and Miranda-Ribera, Alba and Feng, Chiguang and Liu, Anguo and Nguyen, Chinh and Zhang, Lei and Luzina, Irina G and Atamas, Sergei P and Twaddell, William S and Guang, Wei and Lillehoj, Erik P and Puché, Adam C and Huang, Wei and Wang, Lai-Xi and Passaniti, Antonino and Goldblum, Simeon E
Journal of Biological Chemistry, ISSN 0021-9258, 05/2012, Volume 287, Issue 19, pp. 15966 - 15980
The microvascular endothelial surface expresses multiple molecules whose sialylation state regulates multiple aspects of endothelial function. To better... 
B16 MELANOMA-CELLS | HUMAN NEUTROPHILS | LYSOSOMAL SIALIDASE | BIOCHEMISTRY & MOLECULAR BIOLOGY | SURFACE | RECEPTOR | TUMOR-CELLS | GROWTH-FACTOR | ADHESION MOLECULES | SIALYL-LEX | PLASMA-MEMBRANE | Humans | Kidney - enzymology | Neuraminidase - genetics | Substrate Specificity | Immunoblotting | Cell Nucleus - enzymology | Lung - enzymology | Cytosol - enzymology | Hymecromone - analogs & derivatives | Flow Cytometry | RNA Interference | Carotid Arteries - enzymology | Hymecromone - pharmacology | Aorta - enzymology | Cell Line | Endothelial Cells - metabolism | Neuraminidase - metabolism | Reverse Transcriptase Polymerase Chain Reaction | N-Acetylneuraminic Acid - metabolism | Gene Expression Regulation, Enzymologic | Cell Membrane - enzymology | Microscopy, Confocal | Cerebral Arteries - enzymology | N-Acetylneuraminic Acid - analogs & derivatives | Neuraminidase - antagonists & inhibitors | Endothelial Cells - enzymology | Cell Movement | Index Medicus | Sialic Acid | Glycobiology | Signal Transduction | Endothelial Dysfunction | Lung | Vascular Biology | Migration | Neuraminidase | Glycobiology and Extracellular Matrices | Wound Healing | Sialidase
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