Search results for "rho-Associated Kinases"

showing 10 items of 15 documents

Telomere Shortening in Neural Stem Cells Disrupts Neuronal Differentiation and Neuritogenesis

2009

Proliferation in the subependymal zone (SEZ) and neurogenesis in the olfactory bulb decline in the forebrain of telomerase-deficient mice. The present work reveals additional effects of telomere shortening on neuronal differentiation, as adult multipotent progenitors with critically short telomeres yield reduced numbers of neurons that, furthermore, exhibit underdeveloped neuritic arbors. Genetic data indicate that the tumor suppressor protein p53 not only mediates the adverse effects of telomere attrition on proliferation and self-renewal but it is also involved in preventing normal neuronal differentiation of adult progenitors with dysfunctional telomeres. Interestingly, progenitor cells …

AgingTelomeraseRHOANeurogenesisNotch signaling pathwayBiologyMice03 medical and health sciencesFetus0302 clinical medicineNeuritesSubependymal zoneAnimalsTelomeraseCells Cultured030304 developmental biologyMice KnockoutNeuronsrho-Associated Kinases0303 health sciencesReceptors NotchStem CellsGeneral NeuroscienceNeurogenesisCell DifferentiationArticlesTelomereNeural stem cellOlfactory bulbTelomereMice Inbred C57BLAnimals Newbornbiology.proteinTumor Suppressor Protein p53Neuroscience030217 neurology & neurosurgerySignal TransductionThe Journal of Neuroscience
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Inhibitors of Rho-kinase modulate amyloid-β (Aβ) secretion but lack selectivity for Aβ42

2005

Certain non-steroidal anti-inflammatory drugs (NSAIDs) preferentially inhibit production of the amyloidogenic Abeta42 peptide, presumably by direct modulation of gamma-secretase activity. A recent report indicated that NSAIDs could reduce Abeta42 by inhibition of the small GTPase Rho, and a single inhibitor of Rho kinase (ROCK) mimicked the effects of Abeta42-lowering NSAIDs. To investigate whether Abeta42 reduction is a common property of ROCK inhibitors, we tested commercially available compounds in cell lines that were previously used to demonstrate the Abeta42-lowering activity of NSAIDs. Surprisingly, we found that two ROCK inhibitors reduced total Abeta secretion in a dose-dependent m…

Cell SurvivalMutantPeptideCHO CellsProtein Serine-Threonine KinasesPharmacologyBiochemistryAmyloid beta-Protein PrecursorCellular and Molecular NeuroscienceCricetulusCricetinaeEndopeptidasesmental disordersAmyloid precursor proteinAnimalsAspartic Acid EndopeptidasesSecretionSmall GTPaseEnzyme InhibitorsRho-associated protein kinasechemistry.chemical_classificationrho-Associated KinasesAmyloid beta-PeptidesbiologyAnti-Inflammatory Agents Non-SteroidalIntracellular Signaling Peptides and ProteinsIn vitro toxicologyProtein-Tyrosine KinasesPeptide Fragmentsnervous system diseasesBiochemistrychemistrybiology.proteinAmyloid Precursor Protein SecretasesSelectivityProtein Processing Post-TranslationalJournal of Neurochemistry
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Diverse compounds mimic Alzheimer disease–causing mutations by augmenting Aβ42 production

2004

Increased Abeta42 production has been linked to the development of Alzheimer disease. We now identify a number of compounds that raise Abeta42. Among the more potent Abeta42-raising agents identified are fenofibrate, an antilipidemic agent, and celecoxib, a COX-2-selective NSAID. Many COX-2-selective NSAIDs tested raised Abeta42, including multiple COX-2-selective derivatives of two Abeta42-lowering NSAIDs. Compounds devoid of COX activity and the endogenous isoprenoids FPP and GGPP also raised Abeta42. These compounds seem to target the gamma-secretase complex, increasing gamma-secretase-catalyzed production of Abeta42 in vitro. Short-term in vivo studies show that two Abeta42-raising comp…

Enzyme-Linked Immunosorbent AssayEndogenyProtein Serine-Threonine KinasesPharmacologyTransfectionMass SpectrometryGeneral Biochemistry Genetics and Molecular BiologyPresenilinCell LineFenofibrateAlzheimer DiseaseIn vivoEndopeptidasesmedicineAspartic Acid EndopeptidasesHumansImmunoprecipitationCyclooxygenase InhibitorsProtein precursorHypolipidemic AgentsSulfonamidesrho-Associated KinasesAmyloid beta-PeptidesFenofibratebusiness.industryAnti-Inflammatory Agents Non-SteroidalIntracellular Signaling Peptides and ProteinsBrainGeneral Medicinemedicine.diseaseIn vitroEnzyme ActivationBiochemistryCelecoxibPyrazolesFemaleAmyloid Precursor Protein SecretasesAlzheimer's diseaserhoA GTP-Binding ProteinbusinessAntilipidemic Agentmedicine.drugNature Medicine
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Structure–activity relationships, and drug metabolism and pharmacokinetic properties for indazole piperazine and indazole piperidine inhibitors of RO…

2007

ROCK has been implicated in many diseases ranging from glaucoma to spinal cord injury and is therefore an important target for therapeutic intervention. In this study, we have designed a series of 1-(4-(1H-indazol-5-yl)piperazin-1-yl)-2-hydroxy(or 2-amino) analogs and a series of 1-(4-(1H-indazol-5-yl amino)piperidin-1-yl)-2-hydroxy(or 2-amino) inhibitors of ROCK-II. SR-1459 has IC50 = 13 nM versus ROCK-II while the IC50s for SR-715 and SR-899 are 80 nM and 100 nM, respectively. Many of these inhibitors, especially the 2-amino substituted analogs for both series, are modest/potent CYP3A4 inhibitors as well. However, a few of these inhibitors (SR-715 and SR-899) show strong selectivity for R…

KinaseIndazolesInhibitorStereochemistryClinical BiochemistryPharmaceutical ScienceProtein Serine-Threonine KinasesPharmacologyBiochemistryPiperazinesInhibitory Concentration 50Structure-Activity Relationshipchemistry.chemical_compoundDrug StabilityPiperidinesIn vivoDrug DiscoveryAnimalsCytochrome P-450 CYP3ACytochrome P-450 Enzyme InhibitorsHumansStructure–activity relationshipPharmacokineticsRho-kinaseProtein Kinase InhibitorsMolecular BiologyCytochrome P-450 Enzyme Inhibitorsrho-Associated KinasesIndazoleCYP3A4Organic ChemistryIntracellular Signaling Peptides and ProteinsROCK-IIRatsPiperazinePharmaceutical PreparationschemistryMolecular MedicinePiperidineDrug metabolismBioorganic & Medicinal Chemistry Letters : a tetrahedron publication for the rapid dissemination of preliminary communication and all aspects of bioorganic chemistry, medicinal chemistry and related disciplines
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The antifibrotic potential of a sustained release formulation of a PDGF beta-receptor targeted rho kinase inhibitor

2019

Rho kinase activity in hepatic stellate cells (HSCs) is associated with activation, transformation and contraction of these cells, leading to extracellular matrix production and portal hypertension in liver cirrhosis. Inhibition of rho kinase activity can reduce these activities, but may also lead to side effects, for instance systemic hypotension. This can be circumvented by liver-specific delivery of a rho kinase inhibitor to effector cells. Therefore, we targeted the rho kinase inhibitor Y27632 to the key pathogenic cells in liver fibrosis, i.e. myofibroblasts including activated HSCs that highly express the PDGF beta-receptor, using the drug carrier pPB-MSA. This carrier consists of mou…

Liver CirrhosisDrug targetingPyridinesPolymeric microspheresPharmaceutical Science02 engineering and technologyPharmacologychemistry.chemical_compoundY-27632FibrosisControlled releaseRho-associated protein kinaseMice Knockout0303 health sciencesDrug Carriersrho-Associated KinasesChemistryCIRRHOTIC RATS021001 nanoscience & nanotechnologyMicrospheresY-27632Drug deliveryFemale0210 nano-technologyDrug carrierATP Binding Cassette Transporter Subfamily BSIGNALING CONTRIBUTESLiver fibrosisBiologicalsHEPATIC STELLATE CELLSCell LineMECHANISMSReceptor Platelet-Derived Growth Factor beta03 medical and health sciencesDELIVERYROCK INHIBITORmedicineAnimalsHumansProtein Kinase Inhibitors030304 developmental biologyProtein deliveryPORTAL PRESSUREmedicine.diseaseAmidesTargeted drug deliveryRho kinase inhibitorDelayed-Action PreparationsHepatic stellate cellVASODILATIONJournal of Controlled Release
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Membrane-Derived Phospholipids Control Synaptic Neurotransmission and Plasticity

2015

Synaptic communication is a dynamic process that is key to the regulation of neuronal excitability and information processing in the brain. To date, however, the molecular signals controlling synaptic dynamics have been poorly understood. Membrane-derived bioactive phospholipids are potential candidates to control short-term tuning of synaptic signaling, a plastic event essential for information processing at both the cellular and neuronal network levels in the brain. Here, we showed that phospholipids affect excitatory and inhibitory neurotransmission by different degrees, loci, and mechanisms of action. Signaling triggered by lysophosphatidic acid (LPA) evoked rapid and reversible depress…

MalePatch-Clamp TechniquesQH301-705.5NeurotransmissionBiologyInhibitory postsynaptic potentialSynaptic TransmissionGeneral Biochemistry Genetics and Molecular BiologyMicePregnancySynaptic augmentationMetaplasticityAnimalsRats WistarBiology (General)Motor Neuronsrho-Associated KinasesNeuronal PlasticityGeneral Immunology and MicrobiologyCalcineurinGeneral NeuroscienceReceptors GABA-ACell biologySynaptic fatigueBiochemistrySynapsesSynaptic plasticityExcitatory postsynaptic potentialFemalelipids (amino acids peptides and proteins)Synaptic signalingLysophospholipidsrhoA GTP-Binding ProteinGeneral Agricultural and Biological SciencesResearch Article
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Cigarette smoke exposure up-regulates endothelin receptor B in human pulmonary artery endothelial cells: molecular and functional consequences

2010

BACKGROUND AND PURPOSEPulmonary arteries from smokers and chronic obstructive pulmonary disease patients show abnormal endothelium-dependent vascular reactivity. We studied the effect of cigarette smoke extract (CSE) on endothelin receptor B (ETB) expression in human pulmonary artery endothelial cells (HPAECs) and its role in endothelial dysfunction.EXPERIMENTAL APPROACHETB receptor expression was measured by real time RT-PCR, Western blot and immunofluorescence. Cell contraction, intracellular Ca2+, F/G-actin, RhoA activity, myosin light chain phosphorylation, ET, NO, thromboxane (Tx)A2 and reactive oxygen species (ROS) were measured by traction microscopy, fluorescence microscopy, phalloi…

MalePulmonary ArteryNitric OxideTransfectionMuscle Smooth Vascularendothelial dysfunctionendothelin receptor Bpulmonary artery endothelial cellsSmokeTobaccoHumansRNA Small InterferingCells CulturedAgedSulfonamidesrho-Associated KinasesEndothelin-1bosentancigarette smokeEndothelial CellsResearch PapersReceptor Endothelin BUp-RegulationThromboxane B2FemaleEndothelium VascularReactive Oxygen Species
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Sex-dependent changes in the pulmonary vasoconstriction potential of newborn rats following short-term oxygen exposure

2012

Chronic exposure to supplemental oxygen (O(2)) induces lung damage and mortality in a sex-dependent manner. The effect of short-term hyperoxia on the newborn pulmonary vasculature is unknown but is, however, of clinical significance in the neonatal resuscitation context. We hypothesize that short-term hyperoxia has a sex-dependent effect on the pulmonary vasculature.Following 1-h 100% O(2) exposure, the pulmonary arteries and lung tissues of newborn rats were evaluated.Superoxide dismutase 3 (SOD3) expression in female pups' lungs was increased as compared with that in the lungs of male pups. As compared with air-treated pups, the response of male pups to thromboxane was increased by O(2), …

MaleTime FactorsHypertension PulmonaryHyperoxiaPulmonary ArteryRats Sprague-DawleySex FactorsSuperoxidesPeroxynitrous AcidHypoxic pulmonary vasoconstrictionAnimalsVasoconstrictor AgentsMedicineFamilial Primary Pulmonary Hypertensionskin and connective tissue diseasesOXYGEN EXPOSURELungrho-Associated KinasesDose-Response Relationship DrugSuperoxide Dismutasebusiness.industryFree Radical ScavengersHydrogen PeroxideRatsUp-RegulationEnzyme ActivationDisease Models AnimalOxidative StressAnimals NewbornVasoconstrictionAnesthesiaPediatrics Perinatology and Child HealthFemalesense organsbusinessPediatric Research
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Estradiol induces endothelial cell migration and proliferation through estrogen receptor-enhanced RhoA/ROCK pathway

2010

Migration and proliferation of endothelial cells are involved in re-endothelialization and angiogenesis, two important cardiovascular processes that are increased in response to estrogens. RhoA, a small GTPase which controls multiple cellular processes, is involved in the control of cell migration and proliferation. Our aim was to study the role of RhoA on estradiol-induced migration and proliferation and its dependence on estrogen receptors activity. Human umbilical vein endothelial cells were stimulated with estradiol, in the presence or absence of ICI 182780 (estrogen receptors antagonist) and Y-27632 (Rho kinase inhibitor). Estradiol increased Rho GEF-1 gene expression and RhoA (gene an…

MaleTranscriptional ActivationRHOAAngiogenesismedicine.drug_classEstrogen receptorCell Cycle ProteinsBiochemistryUmbilical CordEndocrinologyCell MovementmedicineHumansReceptorMolecular BiologyCells CulturedCell ProliferationEnzyme Assaysrho-Associated KinasesEstradiolbiologyChemistryEndothelial CellsCell migrationUp-RegulationCell biologyEndothelial stem cellReceptors EstrogenRho kinase inhibitorEstrogenCancer researchbiology.proteinFemalerhoA GTP-Binding Proteinhormones hormone substitutes and hormone antagonistsSignal TransductionMolecular and Cellular Endocrinology
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Deficient p27 Phosphorylation at Serine 10 Increases Macrophage Foam Cell Formation and Aggravates Atherosclerosis Through a Proliferation-Independen…

2011

OBJECTIVE: Genetic ablation of the growth suppressor p27(Kip1) (p27) in the mouse aggravates atherosclerosis coinciding with enhanced arterial cell proliferation. However, it is unknown whether molecular mechanisms that limit p27's protective function contribute to atherosclerosis development and whether p27 exerts proliferation-independent activities in the arterial wall. This study aims to provide insight into both questions by investigating the role in atherosclerosis of p27 phosphorylation at serine 10 (p27-phospho-Ser10), a major posttranslational modification of this protein. METHODS AND RESULTS: Immunoblotting studies revealed a marked reduction in p27-phospho-Ser10 in atheroscleroti…

Malerho GTP-Binding ProteinsRHOAMoesinMiceApolipoproteins ERadixinSerinemedicineAnimalsHumansProtein phosphorylationPhosphorylationProtein kinase ACell ProliferationFoam cellMice Knockoutrho-Associated KinasesbiologyArteriesAtherosclerosismedicine.diseaseCell biologyMice Inbred C57BLDisease Models AnimalAtheromaCase-Control StudiesImmunologyDisease Progressionbiology.proteinPhosphorylationFemalerhoA GTP-Binding ProteinCardiology and Cardiovascular MedicineCyclin-Dependent Kinase Inhibitor p27Foam CellsSignal TransductionArteriosclerosis, Thrombosis, and Vascular Biology
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