Search results for "Rho Kinase"

showing 8 items of 8 documents

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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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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Bradykinin Contracts Rat Urinary Bladder Largely Independently of Phospholipase C

2014

Several receptor systems in the bladder causing detrusor smooth muscle contraction stimulate phospholipase C (PLC). PLC inhibition abolishes bladder contraction via P2Y6 but not that via M3 muscarinic receptors, indicating a receptor-dependent role of PLC. Therefore, we explored the role of PLC in rat bladder contraction by bradykinin. The PLC inhibitor U 73,122 [1-(6-[([17β]-3-methoxyestra-1,3,5[10]-trien-17-yl)-amino]hexyl)-1H-pyrrole-2,5-dione] did not affect the bradykinin response to a significantly greater degree than its inactive analog U 73,343 [10 μM each; 1-(6-[-([17β]-3-methoxyestra-1,3,5[10]-trien-17-yl)-amino]hexyl)-2,5-pyrrolidinedione], whereas the phospholipase D inhibitor b…

Malemedicine.medical_specialtyUrinary BladderMedizinBradykininPharmacologyBradykininCyclooxygenase pathwaychemistry.chemical_compoundOrgan Culture TechniquesInternal medicinemedicineAnimalsCalphostinRats WistarBradykinin receptorPharmacologyDose-Response Relationship DrugPhospholipase CMuscle SmoothSmooth muscle contractionRatsChelerythrineEndocrinologychemistryRho kinase inhibitorType C PhospholipasesMolecular MedicineMuscle ContractionJournal of Pharmacology and Experimental Therapeutics
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Plexin-B1 and Semaphorin 4D Cooperate to Promote Perineural Invasion in a RhoA/ROK-Dependent Manner

2012

Perineural invasion (PNI) is a tropism of tumor cells for nerve bundles located in the surrounding stroma. It is a pathological feature observed in certain tumors, referred to as neurotropic malignancies, that severely limits the ability to establish local control of disease and results in pain, recurrent growth, and distant metastases. Despite the importance of PNI as a prognostic indicator, its biological mechanisms are poorly understood. The semaphorins and their receptors, the plexins, compose a family of proteins originally shown to be important in nerve cell adhesion, axon migration, and proper central nervous system development. Emerging evidence has demonstrated that these factors a…

Nervous systemPathologymedicine.medical_specialtyCell typeanimal structuresRHOANervous System NeoplasmsTransplantation HeterologousPerineural invasionRetraction NoticeMice NudeNerve Tissue ProteinsReceptors Cell SurfaceSemaphorinsPathology and Forensic Medicine03 medical and health sciencesMice0302 clinical medicineSemaphorinAntigens CDCell MovementCell Line TumorSettore BIO/10 - BiochimicamedicineAnimalsHumansNeoplasm InvasivenessAxonRNA Small InterferingCell adhesion030304 developmental biologyMice Knockout0303 health sciencesbiologyDrug SynergismAxonsTransplantationMice Inbred C57BLmedicine.anatomical_structure030220 oncology & carcinogenesisembryonic structuresbiology.proteinCancer researchperineural invasion tumor cells Rho kinase-dependent manner plexin B1rhoA GTP-Binding ProteinNeoplasm TransplantationSignal TransductionThe American Journal of Pathology
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Reduction of tumor necrosis factor-alpha (TNF-α) related nuclear factor-kappaB (NF-κB) translocation but not inhibitor kappa-B (Iκ-B)-degradation by …

2002

Degradation of inhibitor kappa-B (Ikappa-B) followed by translocation of nuclear factor-kappaB (NF-kappaB) into the nucleus and activation of gene expression is essential in tumor necrosis factor-alpha (TNF-alpha)-signaling. In order to analyze the role of Rho proteins in TNF-alpha-induced NF-kappaB-activation in human umbilical cord vein endothelial cells (HUVEC) we used Clostridium difficile toxin B-10463 (TcdB-10463) which inactivates RhoA/Rac1/Cdc42 by glucosylation and Clostridium botulinum C3-toxin which inhibits RhoA/B/C by ADP-ribosylation. Exposure of HUVEC to 10 ng/mL TcdB-10463 or 2.5 microg/mL C3-toxin inhibited TNF-alpha (100 ng/mL)-induced expression of a NF-kappaB-dependent r…

PharmacologyTRAF2RHOATumor Necrosis Factor-alphaNF-kappa BClostridium difficile toxin ABiological TransportRAC1Chromosomal translocationDNABiologyBiochemistryMolecular biologyRho kinase inhibitorbiology.proteinHumansI-kappa B ProteinsTumor necrosis factor alphaEndothelium VascularInterleukin 8rhoA GTP-Binding ProteinCells CulturedBiochemical Pharmacology
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The development of benzimidazoles as selective rho kinase inhibitors

2010

Rho Kinase (ROCK) is a serine/threonine kinase whose inhibition could prove beneficial in numerous therapeutic areas. We have developed a promising class of ATP-competitive inhibitors based upon a benzimidazole scaffold, which show excellent potency toward ROCK (IC(50)<10nM). This report details the optimization of selectivity for ROCK over other related kinases such as Protein kinase A (PKA).

Serine/threonine-specific protein kinaserho-Associated KinasesMAP kinase kinase kinaseChemistryKinaseOrganic ChemistryClinical BiochemistryPharmaceutical ScienceGlaucomaChromanMitogen-activated protein kinase kinaseBiochemistryBenzimidazoleBiochemistryDrug DiscoveryROCKMolecular MedicineBenzimidazolesCyclin-dependent kinase 9Protein kinase ARho KinaseProtein Kinase InhibitorsMolecular BiologyRho-associated protein kinaseProtein kinase CBioorganic & 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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Inhibition of intracellular Ca2+ release by a Rho-kinase inhibitor for the treatment of ischemic damage in primary cultured rat hippocampal neurons.

2008

The effects of hydroxy fasudil, a specific Rho-kinase inhibitor, on behavior and brain neuronal activity in animal studies have been described previously. However, whether a Rho-kinase inhibitor can directly protect neurons against ischemic damage and the molecular mechanisms underlying these effects are poorly understood. The present work was designed to investigate the effect of hydroxy fasudil against oxygen-glucose deprivation (OGD) induced acute neuronal injury and the underlying mechanisms in vitro. Pretreatment with hydroxy fasudil at 5 and 10 microM could concentration-dependently improve cell viability and decrease Lactate dehydrogenase (LDH) level in extracellular solution of neur…

medicine.medical_specialtyExcitotoxicityIntracellular SpaceGlutamic AcidBiologymedicine.disease_causeNeuroprotectionHippocampusCalcium in biologyPotassium ChlorideRats Sprague-DawleyCalcium imagingAdenosine TriphosphateIschemiaInternal medicine1-(5-Isoquinolinesulfonyl)-2-MethylpiperazinemedicineAnimalsHypoxiaProtein Kinase InhibitorsCells CulturedPharmacologyNeuronsrho-Associated KinasesDose-Response Relationship DrugCalcium channelFasudilGlutamate receptorRatsEndocrinologyGlucoseRho kinase inhibitorCalciumEuropean journal of pharmacology
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Antiproliferative effects of drugs affecting different signalling pathways on rat and human pulmonary artery smooth muscle cells

2015

Current treatments for pulmonary arterial hypertension (PAH) include pulmonary vasodilators which may also inhibit PASMC proliferation. The aim of this study was to compare the antiproliferative effects of multiple drugs on rat and human PASMC (rPASMC and hPMASC, respectively) in vitro. rPASMCs and hPASMC were starved for 24 h, then treated with different inhibitors and incubated for 48 h in 1% foetal calf serum plus endothelin-1, 5-HT and U46619. Cell number was estimated by the MTT test. Viable cells increased by 160-180% in 48 h. Activation of the cGMP pathway with the soluble guanylyl cyclase activators riociguat and YC-1 (≤ 10 µM) or the cAMP pathway by the adenylyl cyclase activator f…

medicine.medical_specialtyForskolinmedicine.drug_mechanism_of_actionbusiness.industryProstacyclinPharmacologyRiociguatchemistry.chemical_compoundEndocrinologychemistryRho kinase inhibitorInternal medicinemedicinecAMP-dependent pathwayPotassium channel openerSoluble guanylyl cyclasebusinessPhosphodiesterase 5 inhibitormedicine.drug4.3 Pulmonary Circulation and Pulmonary Vascular Disease
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