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PloS one, ISSN 1932-6203, 2014, Volume 9, Issue 10, p. e110766
Journal Article
Journal of Cerebral Blood Flow & Metabolism, ISSN 1559-7016, 2006, 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 | CLAUDIN | ACTIVATION | rat | PERMEABILITY | REPERFUSION | PROTEOLYSIS | BLOOD-BRAIN-BARRIER | NEUROSCIENCES | occludin | STRANDS | 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
Journal Article
Proceedings of the National Academy of Sciences - PNAS, ISSN 0027-8424, 5/2016, Volume 113, Issue 18, pp. E2536 - E2545
Journal Article
Journal Article
Lancet neurology, ISSN 1474-4422, 2009, Volume 8, Issue 7, pp. 643 - 653
Summary Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) is the most common heritable cause of stroke and... 
Neurology | SUBCORTICAL INFARCTS | POSITRON-EMISSION-TOMOGRAPHY | WHITE-MATTER | VASCULAR COGNITIVE IMPAIRMENT | HEREDITARY MULTIINFARCT DEMENTIA | AUTOSOMAL-DOMINANT ARTERIOPATHY | NOTCH3 MUTATIONS | TRANSGENIC MOUSE MODEL | LEUKOENCEPHALOPATHY CADASIL | CONDITION CAUSING STROKE | CLINICAL NEUROLOGY | CADASIL - pathology | Muscle, Smooth, Vascular - metabolism | Humans | Brain Infarction - pathology | Receptors, Notch - genetics | Muscle, Smooth, Vascular - physiopathology | Migraine with Aura - pathology | Brain - blood supply | CADASIL - therapy | Migraine with Aura - physiopathology | Genetic Predisposition to Disease - genetics | Cerebral Arteries - physiopathology | Brain Ischemia - physiopathology | Brain Infarction - physiopathology | Brain Ischemia - etiology | CADASIL - genetics | Disease Progression | Brain Infarction - etiology | Muscle, Smooth, Vascular - pathology | Cerebral Arteries - metabolism | Brain Ischemia - pathology | Cerebral Arteries - pathology | Migraine with Aura - etiology | Brain - pathology | Receptor, Notch3 | Brain damage | Cell research | Cysteine | Migraine | Genetically modified organisms | Dementia | Neuroimaging | Headache | Animal models | Stroke | vascular dementia | Cognitive ability | Clinical trials | Smooth muscle | Arteries | Reviews | Magnetic resonance imaging | Genetic engineering | Notch protein | Mutation | Age
Journal Article
American journal of physiology. Heart and circulatory physiology, ISSN 1522-1539, 2015, Volume 308, Issue 9, pp. H1030 - H1038
Journal Article
British journal of pharmacology, ISSN 0007-1188, 10/2013, Volume 170, Issue 3, pp. 661 - 670
Background and Purpose Transient receptor potential vanilloid type 4 (TRPV4) channels are expressed in brain endothelial cells, but their role in regulating... 
cerebral artery | endothelium | TGF‐β1 | vasodilation | amyloid β peptide | oxidative stress | TGF-β1 | ACTIVATION | amyloid peptide | DEPENDENT DILATION | CONTRACTION | TGF-1 | TRANSFORMING GROWTH-FACTOR-BETA-1 | PHARMACOLOGY & PHARMACY | DYSFUNCTION | ASSOCIATION | BRAIN | TRANSGENIC MICE | TGF-BETA-1 | Oxidative Stress | Humans | Transforming Growth Factor beta1 - metabolism | Endothelium, Vascular - drug effects | Male | Cerebrovascular Disorders - metabolism | Cerebral Arteries - drug effects | Dose-Response Relationship, Drug | TRPV Cation Channels - metabolism | Amyloid beta-Protein Precursor - metabolism | Female | Disease Models, Animal | Cerebrovascular Disorders - physiopathology | Alzheimer Disease - physiopathology | Vasodilator Agents - pharmacology | Signal Transduction | Mice, Inbred C57BL | Endothelium, Vascular - physiopathology | Cerebral Arteries - physiopathology | Mice, Transgenic | Transforming Growth Factor beta1 - genetics | Antioxidants - pharmacology | Amyloid beta-Protein Precursor - genetics | Animals | Cerebral Arteries - metabolism | Endothelium, Vascular - metabolism | Alzheimer Disease - metabolism | Cerebrovascular Disorders - genetics | Mice | Mutation | Vasodilation - drug effects | Alzheimer Disease - genetics | Peptides | Analysis | Amyloid beta-protein | Bone morphogenetic proteins | Acetylcholine | Genetic engineering | Transforming growth factors | Alzheimer's disease | Arteries | Endothelium | Medical research | Rodents | Veins & arteries | Research Papers
Journal Article