Search results for "chloride channels"

showing 10 items of 13 documents

A genome-wide association study identifies two loci associated with heart failure due to dilated cardiomyopathy

2011

Dilated cardiomyopathy (DCM) is a major cause of heart failure with a high familial recurrence risk. So far, the genetics of DCM remains largely unresolved. We conducted the first genome-wide association study (GWAS) to identify loci contributing to sporadic DCM.One thousand one hundred and seventy-nine DCM patients and 1108 controls contributed to the discovery phase. Pools of DNA stratified on disease status, population, age, and gender were constituted and used for testing association of DCM with 517 382 single nucleotide polymorphisms (SNPs). Three DCM-associated SNPs were confirmed by individual genotyping (P5.0 10(-7)), and two of them, rs10927875 and rs2234962, were replicated in ind…

AdultCardiomyopathy DilatedMaleCandidate genemedicine.medical_specialtyHeterozygoteHeart diseaseCardiomyopathyHSP27 Heat-Shock ProteinsMutation MissenseGenome-wide association studySingle-nucleotide polymorphism030204 cardiovascular system & hematologycomplex mixturesPolymorphism Single Nucleotide03 medical and health sciences0302 clinical medicineChloride ChannelsInternal medicinemedicineHumanscardiovascular diseasesComputingMilieux_MISCELLANEOUS030304 developmental biologyAdaptor Proteins Signal TransducingHeart Failure0303 health sciences[SDV.GEN]Life Sciences [q-bio]/GeneticsCLCNKAbiologybusiness.industryChromosomes Human Pair 10Dilated cardiomyopathyMiddle Agedmusculoskeletal systemmedicine.diseaseFasttrack Clinical3. Good healthChromosomes Human Pair 1Genetic LociHeart failurecardiovascular systemCardiologybiology.proteinFemaleCardiology and Cardiovascular MedicinebusinessApoptosis Regulatory ProteinsGenome-Wide Association Study
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ANO1 as a marker of oral squamous cell carcinoma and silencing ANO1 suppresses migration of human scc-25 cells

2013

Objectives: The purpose of this study is to confirm that ANO1 correlates with occurrence and metastasis of OSCC. Study Design: Immunohistochemistry was used to detect the expression of ANO1 in 160 specimens of OSCC and normal tissues. Lentiviral silencing ANO1 was used in scc-25 cell line to study the cell migration and cell detachment. Results: Immunohistochemical staining revealed that ANO1 was expressed in a large majority (132 out of 160, 82.5%) of OSCC specimens and that the rate of ANO1 expression in OSCC was significantly higher than that of normal tissue ( P 0.05). Conclusions: Our study shows that abnormal expression of ANO1 correlated with the occurrence and metastasis of OSCC in …

AdultMalePathologymedicine.medical_specialtyCellOdontologíaBiologyMetastasisCell MovementChloride ChannelsBiomarkers TumorTumor Cells CulturedCarcinomamedicineHumansGene silencingGene SilencingGeneral DentistryAnoctamin-1Chloride channel activityMouth neoplasmOral Medicine and PathologyResearchCell migrationMiddle Aged:CIENCIAS MÉDICAS [UNESCO]medicine.diseaseCiencias de la saludNeoplasm Proteinsstomatognathic diseasesmedicine.anatomical_structureOtorhinolaryngologyUNESCO::CIENCIAS MÉDICASCarcinoma Squamous CellImmunohistochemistryFemaleMouth NeoplasmsSurgeryMedicina Oral Patología Oral y Cirugia Bucal
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Superoxide Flux in Endothelial Cells via the Chloride Channel-3 Mediates Intracellular Signaling

2007

Reactive oxygen species (ROS) have been implicated in both cell signaling and pathology. A major source of ROS in endothelial cells is NADPH oxidase, which generates superoxide (O2.−) on the extracellular side of the plasma membrane but can result in intracellular signaling. To study possible transmembrane flux of O2.−, pulmonary microvascular endothelial cells were preloaded with the O2.−-sensitive fluorophore hydroethidine (HE). Application of an extracellular bolus of O2.−resulted in rapid and concentration-dependent transient HE oxidation that was followed by a progressive and nonreversible increase in nuclear HE fluorescence. These fluorescence changes were inhibited by superoxide dism…

ApoptosisMembrane PotentialsSuperoxide dismutasechemistry.chemical_compoundChloride ChannelsSuperoxidesExtracellularAnimalsHumansEnzyme InhibitorsRNA Small InterferingMolecular BiologyLungCells CulturedFluorescent Dyeschemistry.chemical_classificationReactive oxygen speciesNADPH oxidasebiologySuperoxideAngiotensin IIThrombinAcetophenonesEndothelial CellsNADPH OxidasesCell BiologyArticlesCell biologyMitochondriaPhenanthridinesOxygenchemistryDIDSbiology.proteinCalciumSignal transductionOxidation-ReductionIntracellularSignal Transduction
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Roflumilast inhibits respiratory syncytial virus infection in human differentiated bronchial epithelial cells.

2013

Respiratory syncytial virus (RSV) causes acute exacerbations in COPD and asthma. RSV infects bronchial epithelial cells (HBE) that trigger RSV associated lung pathology. This study explores whether the phosphodiesterase 4 (PDE4) inhibitor Roflumilast N-oxide (RNO), alters RSV infection of well-differentiated HBE (WD-HBE) in vitro. WD-HBE were RSV infected in the presence or absence of RNO (0.1-100 nM). Viral infection (staining of F and G proteins, nucleoprotein RNA level), mRNA of ICAM-1, ciliated cell markers (digital high speed videomicroscopy, β-tubulin immunofluorescence, Foxj1 and Dnai2 mRNA), Goblet cells (PAS), mRNA of MUC5AC and CLCA1, mRNA and protein level of IL-13, IL-6, IL-8, T…

CyclopropanesScienceAminopyridinesBronchiCell CountRespiratory Syncytial Virus InfectionsBiologyMucin 5ACImmunofluorescenceVirus ReplicationVirusAntioxidantsChloride ChannelsTubulinGene expressionmedicineHumansCiliaRNA MessengerRespiratory systemRoflumilastMessenger RNAMetaplasiaMultidisciplinarymedicine.diagnostic_testQRvirus diseasesCell DifferentiationEpithelial CellsForkhead Transcription FactorsAxonemal Dyneinsrespiratory systemViral LoadVirologyMolecular biologyRespiratory Syncytial VirusesOxidative StressViral replicationBenzamidesMedicineCytokinesTumor necrosis factor alphaGoblet CellsReactive Oxygen SpeciesBiomarkersmedicine.drugResearch ArticlePloS one
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Commentary: "Nitric oxide releases Cl(-) from acidic organelles in retinal amacrine cells".

2015

In their recent article (Krishnan and Gleason, 2015) Vijai Krishnan and Evanna Gleason investigate the cellular mechanisms underlying the shift in the GABA reversal potential upon application of nitric oxide (NO). Functional alteration in GABAergic signaling by alterations in the GABA reversal potential has been identified as an important mechanism of plasticity (Raimondo et al., 2012) and NO is clearly one key substance involved in plasticity (Prast and Philippu, 2001). Therefore, the investigation of the mechanisms behind the NO induced shift in GABAergic effects is an important issue. However, in my opinion the authors neglected a possible explanation of their observations in the discuss…

GABAA receptorGeneral CommentaryBafilomycinBiologylcsh:RC321-571Cellular and Molecular Neurosciencechemistry.chemical_compoundCytosolGABAchemistryBiochemistrychloride channelsnitric oxideChloride channelExtracellularBiophysicsGABAergicshort term plasticityReversal potentialnitritelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryIntracellularamacrine cellNeuroscienceFrontiers in cellular neuroscience
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The diversity of GABAA receptors. Pharmacological and electrophysiological properties of GABAA channel subtypes.

1998

The amino acid gamma-aminobutyric-acid (GABA) prevails in the CNS as an inhibitory neurotransmitter that mediates most of its effects through fast GABA-gated Cl(-)-channels (GABAAR). Molecular biology uncovered the complex subunit architecture of this receptor channel, in which a pentameric assembly derived from five of at least 17 mammalian subunits, grouped in the six classes alpha, beta, gamma, delta, sigma and epsilon, permits a vast number of putative receptor isoforms. The subunit composition of a particular receptor determines the specific effects of allosterical modulators of the GABAARs like benzodiazepines (BZs), barbiturates, steroids, some convulsants, polyvalent cations, and et…

Gene isoformMacromolecular SubstancesProtein ConformationProtein subunitNeuroscience (miscellaneous)LoreclezoleConvulsantsBiologyInhibitory postsynaptic potentialGABAA-rho receptorSubstrate SpecificityGABA AntagonistsCellular and Molecular NeuroscienceBenzodiazepinesMiceChloride ChannelsmedicineAnimalsHumansProtein IsoformsReceptorGABA Agonistsgamma-Aminobutyric AcidAnestheticsMice KnockoutBinding SitesIon TransportGABAA receptorReceptors GABA-ARecombinant ProteinsRatsElectrophysiologyNeurologyBiochemistryBarbituratesSteroidsHeterologous expressionIon Channel Gatingmedicine.drugMolecular neurobiology
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Swelling of glial cells in lactacidosis and by glutamate: significance of Cl(-)-transport.

1993

Swelling of glial and nerve cells is characteristic of brain damage in cerebral ischemia or trauma. The therapeutical efficiency of inhibition of Cl(-)-transport by a novel antagonist, the diuretic torasemide, on cytotoxic swelling of glial cells from lactacidosis, or glutamate was analyzed. Lactacidosis and the interstitial accumulation of glutamate are hallmarks of the pathophysiological alterations in ischemic or traumatic brain tissue. C6 glioma cells harvested from culture and suspended in a physiological medium were either exposed to pH 6.2, or 5.0 by lactic acid, or exposed to 1 mM glutamate at normal pH. Cell swelling and viability were quantified by flow cytometry. Lactacidosis of …

IschemiaGlutamic AcidBrain EdemaPharmacologyIon Channelschemistry.chemical_compoundChloridesGlutamatesChloride ChannelsmedicineTumor Cells CulturedAnimalsDiureticsMolecular BiologyAcidosisCell SizeSulfonamidesIon TransportChemistryGeneral NeuroscienceGlutamate receptorMembrane ProteinsGlutamic acidmedicine.diseaseTorsemideLactic acidRatsmedicine.anatomical_structureBiochemistryCell cultureNeurogliaAcidosis LacticNeurology (clinical)Swellingmedicine.symptomNeurogliaDevelopmental BiologyBrain research
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Changes in the expression of cation-Cl- cotransporters, NKCC1 and KCC2, during cortical malformation induced by neonatal freeze-lesion.

2007

Focal cortical malformations comprise a heterogeneous group of disturbances in brain development, often associated with intractable epilepsy. A focal freeze-lesion of cerebral cortex in newborn rat produces a cortical malformation that resembles human polymicrogyria, clinical conditions that results from abnormal neuronal migration. The change in GABAergic functions that occurs during early brain development is induced by an alteration in Cl(-) homeostasis and plays important roles in neocortical development by modulating such events as laminar organization and synaptogenesis. We therefore investigated the relationship between pathogenesis of polymicrogyria and ontogeny of Cl(-) homeostasis…

MaleSodium-Potassium-Chloride SymportersSynaptogenesisDown-RegulationBiologyNervous System MalformationsLaminar organizationChloridesCell MovementChloride ChannelsCortex (anatomy)Parietal LobeGlial Fibrillary Acidic ProteinmedicinePolymicrogyriaAnimalsSolute Carrier Family 12 Member 2RNA MessengerRats Wistargamma-Aminobutyric AcidCerebral CortexSymportersGeneral NeuroscienceColocalizationCell DifferentiationGeneral Medicinemedicine.diseaseDenervationImmunohistochemistryMicrogyrusRatsUp-RegulationCold Temperaturemedicine.anatomical_structureNeuronal migration disorderBromodeoxyuridineCerebral cortexPhosphopyruvate HydrataseNeuroscienceBiomarkersNeuroscience research
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Activation by Acidic pH of CLC-7 Expressed in Oocytes from Xenopus laevis

2002

ClC chloride channels are important in diverse physiological functions such as transepithelial transport, cell volume regulation, excitability, and acidification of intracellular organelles. We have investigated the expression of CLC-7 in oocytes from Xenopus laevis with the two electrode voltage clamp technique and Western blot analysis. Using a specific antibody against CLC-7, we found an approximately 80 kDa protein in oocytes, previously injected with CLC-7-cRNA. In voltage clamp experiments on ClC-7-cRNA-injected oocytes, no current changes were detected at normal pH (7.4). However, acidification of the Ringer solution to pH values between 6 and 4 revealed strong currents which reverse…

Patch-Clamp TechniquesVoltage clampBlotting WesternBiophysicsXenopusBiologyBiochemistryChlorideXenopus laevisWestern blotChloride ChannelsmedicineAnimalsPatch clampMolecular Biologymedicine.diagnostic_testurogenital systemElectric ConductivityCell BiologyHydrogen-Ion Concentrationbiology.organism_classificationMolecular biologyResting potentialRatsBlotOocytesChloride channelBiophysicsmedicine.drugBiochemical and Biophysical Research Communications
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Activation of alpha-1A adrenoceptors mobilizes calcium from the intracellular stores in myocytes from rat portal vein.

1994

International audience; Intracellular free Ca++ concentration ([Ca++]i) was monitored using the fluorescence from the dye fura-2-acetoxymethylester in single myocytes from rat portal vein. In the presence of oxodipine (a L-type Ca++ channel inhibitor), norepinephrine (10 microM) evoked transient increases in [Ca++]i which were related to release of Ca++ from intracellular stores. The alpha-1 adrenoceptors mediating intracellular Ca++ release and inositol phosphate accumulation were identified by using subtype-selective agonists and antagonists. Pretreatment with chloroethylclonidine had little effect on the norepinephrine-induced increase in [Ca++]i and inositol phosphate accumulation. In c…

Portal VeinInositol Phosphates[SDV]Life Sciences [q-bio]Molecular Sequence Data[SDV.BC]Life Sciences [q-bio]/Cellular Biology[SDV.BC.BC]Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]In Vitro TechniquesAntibodiesMuscle Smooth VascularRats[SDV] Life Sciences [q-bio]NorepinephrineChloride ChannelsReceptors Adrenergic alpha-1[SDV.BC.BC] Life Sciences [q-bio]/Cellular Biology/Subcellular Processes [q-bio.SC]AnimalsCalciumAmino Acid SequenceRats Wistar[SDV.BC] Life Sciences [q-bio]/Cellular BiologyAdrenergic alpha-AntagonistsCells CulturedSignal Transduction
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