Search results for "Myosin-Light-Chain Kinase"

showing 3 items of 3 documents

Cellular mechanisms of IL-17-induced blood-brain barrier disruption.

2009

Recently T-helper 17 (Th17) cells were demonstrated to disrupt the blood-brain barrier (BBB) by the action of IL-17A. The aim of the present study was to examine the mechanisms that underlie IL-17A-induced BBB breakdown. Barrier integrity was analyzed in the murine brain endothelial cell line bEnd.3 by measuring the electrical resistance values using electrical call impedance sensing technology. Furthermore, in-cell Western blots, fluorescence imaging, and monocyte adhesion and transendothelial migration assays were performed. Experimental autoimmune encephalomyelitis (EAE) was induced in C57BL/6 mice. IL-17A induced NADPH oxidase- or xanthine oxidase-dependent reactive oxygen species (ROS)…

1303 BiochemistryEncephalomyelitisOccludin10263 Institute of Experimental ImmunologyBiochemistryMice0302 clinical medicineEnzyme InhibitorsCell Line Transformed0303 health sciencesMice Inbred BALB CNADPH oxidasebiologyTight junctionExperimental autoimmune encephalomyelitisInterleukin-17AzepinesT-Lymphocytes Helper-InducerCell biologyEndothelial stem cellBlood-Brain Barrier1305 BiotechnologyBiotechnologyXanthine OxidaseMyosin light-chain kinaseEncephalomyelitis Autoimmune ExperimentalDown-Regulation610 Medicine & healthNaphthalenes03 medical and health sciences1311 GeneticsOccludinGeneticsmedicine1312 Molecular BiologyAnimalsMolecular BiologyMyosin-Light-Chain KinaseNeuroinflammation030304 developmental biologyEndothelial CellsMembrane ProteinsNADPH Oxidasesmedicine.diseaseMolecular biologyAntibodies NeutralizingOxidative Stressbiology.protein570 Life sciences; biologyReactive Oxygen Species030217 neurology & neurosurgeryFASEB journal : official publication of the Federation of American Societies for Experimental Biolog
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Inhibition of myosin light chain kinase reduces brain edema formation after traumatic brain injury.

2010

The role of the endothelial contractile apparatus in the process of brain edema formation after brain trauma is not characterized. Phosphorylation of myosin light chains by myosin light chain kinases (MLCK) activates endothelial contractile elements and results in a rearrangement of the cytoskeleton. This may enhance post-traumatic blood-brain barrier dysfunction. In order to investigate the role of the MLCK on brain edema formation and blood-brain barrier permeability after brain injury, mice were anesthetized and subjected to a controlled cortical impact (CCI). MLCK expression is significantly up-regulated after CCI with a maximum 12 h post-injury. Specific inhibition of MLCK by ML-7 resu…

MaleMyosin light-chain kinaseMyosin Light ChainsTime FactorsEndotheliumIntracranial PressureTraumatic brain injuryCentral nervous systemBrain Edemamacromolecular substancesBrain damageNaphthalenesBlood–brain barrierBiochemistryNeuroprotectionDrug Administration ScheduleFunctional LateralityStatistics NonparametricCerebral edemaCellular and Molecular NeuroscienceMicemedicineAnimalsEnzyme InhibitorsMyosin-Light-Chain KinaseNeurologic Examinationbusiness.industryAzepinesmedicine.diseaseConstrictionCell biologyMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureGene Expression RegulationBlood-Brain BarrierBrain Injuriesmedicine.symptombusinessNeuroscienceEvans BlueJournal of neurochemistry
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The Blood–Brain Barrier as a Target in Traumatic Brain Injury Treatment

2014

Traumatic brain injury (TBI) is one of the most frequent causes of death in the young population. Several clinical trials have unsuccessfully focused on direct neuroprotective therapies. Recently immunotherapeutic strategies shifted into focus of translational research in acute CNS diseases. Cross-talk between activated microglia and blood–brain barrier (BBB) could initiate opening of the BBB and subsequent recruitment of systemic immune cells and mediators into the brain. Stabilization of the BBB after TBI could be a promising strategy to limit neuronal inflammation, secondary brain damage and acute neurodegeneration. This review provides an overview on the pathophysiology of TBI and brain…

Pathologymedicine.medical_specialtyTraumatic brain injuryPeroxisome Proliferator-Activated ReceptorsBrain EdemaInflammationBrain damageBlood–brain barrierNeuroprotectionRosiglitazoneReceptors GlucocorticoidmedicineHumansHypoglycemic AgentsMyosin-Light-Chain KinaseNeuroinflammationInflammationPioglitazoneMicrogliabusiness.industryNeurodegenerationNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseCell HypoxiaNeuroprotective Agentsmedicine.anatomical_structurenervous systemBlood-Brain BarrierBrain InjuriesThiazolidinedionesmedicine.symptombusinessNeuroscienceArchives of Medical Research
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