Search results for "Connexin"

showing 10 items of 59 documents

How miR-31-5p and miR-33a-5p Regulates SP1/CX43 Expression in Osteoarthritis Disease: Preliminary Insights

2021

Osteoarthritis (OA) is a degenerative bone disease that involved micro and macro-environment of joints. To date, there are no radical curative treatments for OA and novel therapies are mandatory. Recent evidence suggests the role of miRNAs in OA progression. In our previous studies, we demonstrated the role of miR-31-5p and miR-33a families in different bone regeneration signaling. Here, we investigated the role of miR-31-5p and miR-33a-5p in OA progression. A different expression of miR-31-5p and miR-33a-5p into osteoblasts and chondrocytes isolated from joint tissues of OA patients classified in based on different Kellgren and Lawrence (KL) grading was highlighted

Male0301 basic medicineBone diseasechondrocytesOsteoarthritisCX43lcsh:Chemistry0302 clinical medicinelcsh:QH301-705.5Cells CulturedSpectroscopymicroRNAosteoblastsGeneral MedicineMiddle AgedPrognosisComputer Science ApplicationsmicroRNAsmir-31030220 oncology & carcinogenesischondrocyteosteoblastFemalemedicine.symptomSignal TransductionAdultSp1 Transcription FactorInflammationBiologyArticleCatalysisInorganic Chemistry03 medical and health sciencesmicroRNAmedicineHumansPhysical and Theoretical ChemistryBone regenerationMolecular BiologyGeneLoss functionAgedOrganic Chemistrymedicine.diseaseSP1osteoarthritis030104 developmental biologyGene Expression Regulationlcsh:Biology (General)lcsh:QD1-999Connexin 43Cancer researchFollow-Up StudiesInternational Journal of Molecular Sciences
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Active acetylcholine receptors prevent the atrophy of skeletal muscles and favor reinnervation

2020

Denervation of skeletal muscles induces severe muscle atrophy, which is preceded by cellular alterations such as increased plasma membrane permeability, reduced resting membrane potential and accelerated protein catabolism. The factors that induce these changes remain unknown. Conversely, functional recovery following denervation depends on successful reinnervation. Here, we show that activation of nicotinic acetylcholine receptors (nAChRs) by quantal release of acetylcholine (ACh) from motoneurons is sufficient to prevent changes induced by denervation. Using in vitro assays, ACh and non-hydrolysable ACh analogs repressed the expression of connexin43 and connexin45 hemichannels, which prom…

Male0301 basic medicineCell Membrane PermeabilityNeuromuscular transmissionSkeletal muscleGeneral Physics and AstronomylihaksetasetyylikoliiniReceptors NicotinicConnexinsMembrane PotentialsMice0302 clinical medicineGanglia SpinalMyocytevälittäjäaineetlcsh:ScienceCells CulturedDenervationMultidisciplinaryChemistryQMuscle atrophy3. Good healthCell biologyMuscular AtrophyNicotinic agonistmedicine.anatomical_structuremedicine.symptomAcetylcholinemedicine.drugReinnervationScienceMice TransgenicArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesmedicineAnimalsskeletal muscleMuscle SkeletalAcetylcholine receptorsoluviestintäsomatic systemGeneral ChemistryAcetylcholineMice Inbred C57BLhermosolut030104 developmental biologynervous systemConnexin 43lcsh:Qsense organsSomatic systemlihassurkastumasairaudet030217 neurology & neurosurgeryNature Communications
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Telmisartan cardioprotects from the ischaemic/hypoxic damage through a miR‐1‐dependent pathway

2019

The aim of this study was to investigate whether telmisartan protects the heart from the ischaemia/reperfusion damage through a local microRNA-1 modulation. Studies on the myocardial ischaemia/reperfusion injury in vivo and on the cardiomyocyte hypoxia/reoxygenation damage in vitro were done. In vivo, male Sprague-Dawley rats administered for 3 weeks with telmisartan 12 mg/kg/d by gastric gavage underwent ischaemia/reperfusion of the left descending coronary artery. In these rats, infarct size measurement, ELISA, immunohistochemistry (IHC) and reverse transcriptase real-time polymerase chain reaction showed that expressions of connexin 43, potassium voltage-gated channel subfamily Q member …

Male0301 basic medicineCell SurvivalMyocardial InfarctionIschemiaConnexinMyocardial Reperfusion InjuryPharmacologymiR‐1telmisartanCell Lineconnexin 43Rats Sprague-Dawleyhypoxic H9c2 cells03 medical and health sciences0302 clinical medicineIn vivomedicineAnimalsBcl-2Myocytes CardiacKCNQ1ChemistryBcl‐2Original ArticlesCell BiologyTransfectionHypoxia (medical)medicine.diseasemiR-1Cell HypoxiaIn vitroRatsMicroRNAsmyocardial ischaemia/reperfusion030104 developmental biologyProto-Oncogene Proteins c-bcl-2030220 oncology & carcinogenesisKCNQ1 Potassium ChannelMolecular Medicinehypoxic H9c2 cellOriginal Articlemedicine.symptomTelmisartanReperfusion injurymedicine.drugJournal of Cellular and Molecular Medicine
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Connexin-30 mRNA Is Up-Regulated in Astrocytes and Expressed in Apoptotic Neuronal Cells of Rat Brain Following Kainate-Induced Seizures

2002

Glial connexins (Cxs) make an extensively interconnected functional syncytium created by a network of gap junctions between astrocytes and oligodendrocytes. Among Cxs expressed in the brain, Cx30 is expressed in grey matter astrocytes, as shown at the protein level by immunoistochemistry. In the present study we aimed to perform a detailed study of the regional distribution of Cx30 mRNA in the adult and postnatal developing rat brain, analyzing its expression by in situ hybridization, and determining its cell type localization by double labeling. Recently, it has been suggested that neuronal activity may control the level of intercellular communication between astrocytes through gap junctio…

MaleAgingCell typeGene ExpressionConnexinApoptosisKainate receptorCell CommunicationIn situ hybridizationGrey matterBiologyConnexinsCellular and Molecular NeuroscienceStatus EpilepticusSeizuresExcitatory Amino Acid AgonistsmedicineAnimalsPremovement neuronal activityRNA MessengerRats WistarMolecular BiologyNeuronsSyncytiumKainic AcidGap junctionBrainCell BiologyImmunohistochemistryRatsUp-RegulationCell biologymedicine.anatomical_structureAnimals NewbornAstrocytesNeuroscienceMolecular and Cellular Neuroscience
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Cellular expression of connexins in the rat brain: neuronal localization, effects of kainate-induced seizures and expression in apoptotic neuronal ce…

2003

The identification of connexins (Cxs) expressed in neuronal cells represents a crucial step for understanding the direct communication between neurons and between neuron and glia. In the present work, using a double-labelling method combining in situ hybridization for Cx mRNAs with immunohistochemical detection for neuronal markers, we provide evidence that, among cerebral connexins (Cx26, Cx32, Cx36, Cx37, Cx40, Cx43, Cx45 and Cx47), only Cx45 and Cx36 mRNAs are localized in neuronal cells in both developing and adult rat brain. In order to establish whether connexin expression is influenced in vivo by abnormal neuronal activity, we examined the short-term effects of kainate-induced seizur…

MaleAgingTime FactorsgliaHippocampusConnexinbrain developmentKainate receptorApoptosisIn situ hybridizationBiologyConnexinsgap junctionbrain development; gap junction; gliaSeizuresTubulinmedicineExcitatory Amino Acid AgonistsIn Situ Nick-End LabelingPremovement neuronal activityAnimalsRNA MessengerOrganic ChemicalsRats WistarIn Situ HybridizationFluorescent DyesNeuronsMessenger RNAKainic AcidReverse Transcriptase Polymerase Chain ReactionGeneral NeuroscienceGap junctionBrainGene Expression Regulation DevelopmentalFluoresceinsImmunohistochemistryCell biologyRatsmedicine.anatomical_structurenervous systemAnimals NewbornPhosphopyruvate HydrataseAutoradiographysense organsNeuronNeuroscienceDensitometryThe European journal of neuroscience
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Anticonvulsant effects of carbenoxolone in genetically epilepsy prone rats (GEPRs).

2004

Carbenoxolone (CBX), the succinyl ester of glycyrrhetinic acid, is an inhibitor of gap junctional intercellular communication. Systemic administration of CBX was able to decrease the seizure severity score and to increase the latency time of seizure onset in genetically epilepsy prone rats (GEPRs). In particular, intravenous or intraperitoneal administration of carbenoxolone (5-30 mg/kg) produced a dose-dependent and significant reduction in the clonic and tonic phases of the audiogenic seizures in GEPRs. The anticonvulsant doses were not associated with an impairment of motor coordination. The bilateral microinjection of CBX (0.001-0.50 microg/0.5 microl) into the inferior colliculi, the s…

MaleAudiogenic seizuremedicine.medical_treatmentGap junctionGEPR-9sCarbenoxoloneSubstantia nigraPharmacologyConnexinConnexinsRats Sprague-DawleyCellular and Molecular NeuroscienceEpilepsyMedicineAnimalsMicroinjectionPharmacologyEpilepsybusiness.industrymedicine.diseaseMotor coordinationRatsAnticonvulsantAnesthesiaSystemic administrationCarbenoxoloneAnticonvulsantsFemalebusinessPars reticulataGEPR-3medicine.drugNeuropharmacology
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CONNEXIN43 GAP JUNCTION LEVELS DURING DEVELOPMENT OF THE THORACIC AORTA ARE TEMPORALLY CORRELATED WITH ELASTIC LAMINAE DEPOSITION AND INCREASED BLOOD…

1997

A characteristic property of the vascular smooth muscle cell is its ability to modulate between a contractile phenotype, responsible for control of vascular tone, through to a synthetic phenotype, capable of migration and synthesis of extracellular matrix molecules. Smooth muscle cells are coupled by gap junctions, the membrane structures which permit direct intercelluar passage of ions and small molecules, and which play a role both in electrical coupling and intercellular communication during patterning and development. We have previously found that connexin43 type gap junction expression is upregulated in the synthetic phenotype smooth muscle cell in vitro and during atherosclerotic plaq…

MaleCell signalingVascular smooth muscleAorta ThoracicBlood PressureCell CommunicationMuscle Smooth VascularRats Sprague-Dawleymedicine.arterymedicineAnimalsThoracic aortaAortaChemistryCell growthGap junctionGap JunctionsCell BiologyGeneral MedicineAnatomyPhenotypeRatsCell biologyConnexin 43FemaleIntracellularCell Biology International
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Expression of connexin36 in the adult and developing rat brain.

2000

The distribution of connexin36 (Cx36) in the adult rat brain and retina has been analysed at the protein (immunofluorescence) and mRNA (in situ hybridization) level. Cx36 immunoreactivity, consisting primarily of round or elongated puncta, is highly enriched in specific brain regions (inferior olive and the olfactory bulb), in the retina, in the anterior pituitary and in the pineal gland, in agreement with the high levels of Cx36 mRNA in the same regions. A lower density of immunoreactive puncta can be observed in several brain regions, where only scattered subpopulations of cells express Cx36 mRNA. By combining in situ hybridization for Cx36 mRNA with immunohistochemistry for a general neu…

MaleCerebellumPathologymedicine.medical_specialtygenetic structuresHippocampusIn situ hybridizationBiologyPineal GlandConnexinsmedicineAnimalsRNA MessengerEye ProteinsMolecular BiologyNeuronsBrain MappingGeneral NeuroscienceAge FactorsBrainGap JunctionsNuclear ProteinsImmunohistochemistryOlfactory bulbCell biologyRatsmedicine.anatomical_structureParvalbuminsnervous systemAnimals NewbornCerebral cortexCerebellar cortexPituitary Glandbiology.proteinsense organsNeurology (clinical)NeuronNeuNBiomarkersDevelopmental BiologyBrain research
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Deficient membrane integration of the novel p.N14D-GJB2mutant associated with non-syndromic hearing impairment

2006

Mutations in GJB2, the gene encoding for the Gap Junction protein Connexin 26 (Cx26), have been established as the major cause of hereditary, non-syndromic hearing impairment (HI). We report here the identification of a novel point mutation in GJB2, c.40A>G [p.N14D], detected in compound heterozygosity with the c.35delG mutation in two brothers with moderate non-syndromic sensorineural HI. The mother who carried one wildtype and a p.N14D allele displayed normal hearing. The mutation leads to substitution of the neutral amino acid asparagine (N) by the negatively charged aspartic acid (D) at amino acid number 14, a position that is conserved among Cx26 of different organisms and among many o…

MaleDNA Mutational AnalysisMutantGene ExpressionConnexinIn Vitro TechniquesBiologymedicine.disease_causeCompound heterozygosityConnexinsXenopus laevisAspartic acidotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansCloning MolecularChildHearing LossGenetics (clinical)chemistry.chemical_classificationMutationPoint mutationCell MembraneWild typeGap JunctionsMolecular biologyPedigreeAmino acidConnexin 26Protein TransportchemistryChild PreschoolAntigens SurfaceMutationOocytesHuman Mutation
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Mild Aerobic Exercise Training Hardly Affects the Diaphragm of mdx Mice

2016

In the mdx mice model of Duchenne Muscular Dystrophy (DMD), mild endurance exercise training positively affected limb skeletal muscles, whereas few and controversial data exist on the effects of training on the diaphragm. The diaphragm was examined in mdx (C57BL/10ScSn-Dmdmdx) and wild-type (WT, C57BL/10ScSc) mice under sedentary conditions (mdx-SD, WT-SD) and during mild exercise training (mdx-EX, WT-EX). At baseline, and after 30 and 45 days (training: 5 d/wk for 6 weeks), diaphragm muscle morphology and Cx39 protein were assessed. In addition, tissue levels of the chaperonins Hsp60 and Hsp70 and the p65 subunit of nuclear factor-kB (NF-kB) were measured in diaphragm, gastrocnemius, and q…

MaleDuchenne muscular dystrophychaperoninTime FactorsDiaphragmSettore MED/10 - Malattie Dell'Apparato RespiratorioSettore BIO/09 - FisiologiaConnexinsMitochondrial ProteinsNecrosisendurance trainingAnimalsGenetic Predisposition to DiseaseHSP70 Heat-Shock Proteinsstress markersMuscle StrengthNF-kBSettore BIO/16 - Anatomia UmanaTranscription Factor RelAChaperonin 60Settore CHIM/06 - Chimica OrganicaExercise TherapyMuscular Dystrophy DuchenneDisease Models AnimalPhenotypeMice Inbred mdxPhysical Endurance
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