Search results for "connexin 43"

showing 10 items of 15 documents

Cardiac electrical defects in progeroid mice and Hutchinson-Gilford progeria syndrome patients with nuclear lamina alterations

2016

This work was supported by Spanish Ministry of Economy and Competitiveness (MINECO) Grants SAF2010-16044 and SAF2013-46663-R (to V.A.), SAF2011-30312 and SAF2014-58286-C2-1-R (to L.H.-M.), SAF2011-30088 (to E.D.), and SAF2014-52413-R (to C.L.-O.) and Fondo de Investigación Sanitaria del Instituto de Salud Carlos III Grants RD12/0042/0028 (to V.A.), RD12/0042/0011 (to J.T.), and RD12/0042/0002 (to L.H.-M.), with cofunding from the Fondo Europeo de Desarrollo Regional and the Progeria Research Foundation. J.A.G. is the recipient of a U-Mobility Grant from the Marie Curie cofunding of Regional, National and International Programme (Grant 246550). The Instituto Universitario de Oncología is sup…

0301 basic medicineMaleHutchinson–Gilford progeria syndrome calcium handling connexin43 prelamin A progerinElectrònica en cardiologia030204 cardiovascular system & hematologyPathogenesisCiencias Biomedicas0302 clinical medicineProgeriaCardiac Conduction System DiseasefisiologiapatologíaTecnología médicaChildCiencias médicasMice KnockoutProgeriaprelamin AMultidisciplinaryintegumentary systemMetalloendopeptidasesHeartProgerinHutchinson-Gilford progeria syndrome3. Good health:Enginyeria biomèdica::Electrònica biomèdica::Electrònica en cardiologia [Àrees temàtiques de la UPC]Sarcoplasmic Reticulummedicine.anatomical_structurePNAS PlusChild Preschoolcardiovascular systemNuclear laminaFemalemedicine.symptomBradycardiaAdultmedicine.medical_specialtycongenital hereditary and neonatal diseases and abnormalitiesAdolescentBiology03 medical and health sciencesQRS complexYoung AdultElectrònica mèdicaInternal medicinemedicineAnimalsHumansPR intervalHutchinson–Gilford progeria syndromeNuclear LaminaMyocardiumMembrane Proteinsnutritional and metabolic diseasesArrhythmias Cardiacmedicine.diseaseMedical electronicsconnexin43Mice Inbred C57BL030104 developmental biologyEndocrinologyVentricleprogerinConnexin 43calcium handlingsistema cardiovascularCalcium
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All-trans retinoic acid restores gap junctional intercellular communication between oral cancer cells with upregulation of Cx32 and Cx43 expressions …

2012

Objective: All-trans retinoic acid (ATRA) has been demonstrated to inhibit tumor growth by restoration of gap junctional intercellular communication (GJIC) via upregulation of connexin (Cx) expression in some solid tumors. However, the relationship between ATRA and GJIC remains unclear in oral squamous cell carcinoma (OSCC). The aim of this study was to investigate the effect of ATRA on the GJIC function of OSCC. Study design: We measured the effects of ATRA on the viability and cell cycle distribution of SCC9 and Tca8113 OSCC cells. The GJIC function was observed using the scrape-loading dye transfer technique, and the mRNA and protein levels of Cx32 and Cx43 were detected by qRT-PCR, West…

Cell cycle checkpointRetinoic acidConnexinAntineoplastic AgentsTretinoinOdontologíaCell CommunicationConnexinschemistry.chemical_compoundDownregulation and upregulationTretinoinmedicineTumor Cells CulturedHumansRNA MessengerGeneral DentistryneoplasmsMouth neoplasmOral Medicine and Pathologyorganic chemicalsGap JunctionsCell cycle:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludbiological factorsUp-RegulationGene Expression Regulation Neoplasticstomatognathic diseasesOtorhinolaryngologychemistryConnexin 43ImmunologyCancer cellUNESCO::CIENCIAS MÉDICASCancer researchCarcinoma Squamous CellSurgeryMouth NeoplasmsResearch-Articlemedicine.drug
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Arsenic trioxide alters the differentiation of mouse embryonic stem cell into cardiomyocytes

2015

AbstractChronic arsenic exposure is associated with increased morbidity and mortality for cardiovascular diseases. Arsenic increases myocardial infarction mortality in young adulthood, suggesting that exposure during foetal life correlates with cardiac alterations emerging later. Here, we investigated the mechanisms of arsenic trioxide (ATO) cardiomyocytes disruption during their differentiation from mouse embryonic stem cells. Throughout 15 days of differentiation in the presence of ATO (0.1, 0.5, 1.0 μM) we analysed: the expression of i) marker genes of mesoderm (day 4), myofibrillogenic commitment (day 7) and post-natal-like cardiomyocytes (day 15); ii) sarcomeric proteins and their orga…

Fetal ProteinsSarcomeresMesodermTime FactorsCellular differentiationBlotting WesternConnexinFluorescent Antibody TechniqueGene ExpressionAntineoplastic AgentsActininBiologyArticleArsenicalsCell Linechemistry.chemical_compoundMiceArsenic TrioxideTroponin TSpheroids CellularGene expressionmedicineAnimalsActininMyocytes CardiacArsenic trioxideHomeodomain ProteinsSyncytiumMultidisciplinaryReverse Transcriptase Polymerase Chain ReactionCell DifferentiationMouse Embryonic Stem CellsOxidesEmbryonic stem cellCell biologyBiomechanical PhenomenaGATA4 Transcription Factormedicine.anatomical_structurechemistryConnexin 43ImmunologyHomeobox Protein Nkx-2.5T-Box Domain ProteinsTroponin CTranscription FactorsScientific Reports
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Correction: Oncogenic extracellular HSP70 disrupts the gap-junctional coupling between capillary cells

2021

High levels of circulating heat shock protein 70 (HSP70) are detected in many cancers. In order to explore the effects of extracellular HSP70 on human microvascular endothelial cells (HMEC), we initially used gap-FRAP technique. Extracellular human HSP70 (rhHSP70), but not rhHSP27, blocks the gap-junction intercellular communication (GJIC) between HMEC, disrupts the structural integrity of HMEC junction plaques, and decreases connexin43 (Cx43) expression, which correlates with the phosphorylation of Cx43 serine residues. Further exploration of these effects identified a rapid transactivation of the Epidermal Growth Factor Receptor in a Toll-Like Receptor 4-dependent manner, preceding its in…

Junctional couplingChemistryCapillary actionCorrectionEndothelial CellsGap JunctionsCell CommunicationRecombinant ProteinsHsp70OncologyConnexin 43BiophysicsExtracellularHumansHSP70 Heat-Shock ProteinsPhosphorylationOncotarget
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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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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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Hypothalamic Astroglial Connexins are Required for Brain Glucose Sensing-Induced Insulin Secretion

2014

Supplementary Information accompanies the paper on the Journal of Cerebral Blood Flow & Metabolism website; Hypothalamic glucose detection participates in maintaining glycemic balance, food intake, and thermogenesis. Although hypothalamic neurons are the executive cells involved in these responses, there is increasing evidence that astrocytes participate in glucose sensing (GS); however, it is unknown whether astroglial networking is required for glucose sensitivity. Astroglial connexins 30 and 43 (Cx30 and Cx43) form hexameric channels, which are apposed in gap junctions, allowing for the intercellular transfer of small molecules such as glucose throughout the astroglial networks. Here, we…

MaleINVOLVEMENTHOMEOSTASISmedicine.medical_specialtymedicine.medical_treatmentNerve Tissue ProteinsCarbohydrate metabolismBiologyASTROCYTESConnexinsconnexin 43RATSastrocyteInternal medicineInsulin SecretionmedicineAnimalsInsulinTANYCYTESRats WistarhypothalamusIN-VIVOHEMICHANNELSglucose sensingInsulinARCUATE NUCLEUSGap junctionFasting[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismBARRIERconnexin 30NETWORKSGlucoseEndocrinologymedicine.anatomical_structureNeurologyHypothalamus[ SDV.NEU ] Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]RNA InterferenceOriginal Article[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]sense organsNeurology (clinical)Cardiology and Cardiovascular MedicineThermogenesisIntracellularHomeostasisAstrocyteJournal of Cerebral Blood Flow & Metabolism
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Regulation of connexin gene expression during skeletal muscle regeneration in the adult rat

2009

In the adult skeletal muscle, various kinds of trauma promote proliferation of satellite cells that differentiate into myoblasts forming new myofibers or to repair the damaged one. The aim of present work was to perform a comparative spatial and temporal analysis of connexin (Cx) 37, Cx39, Cx40, Cx43, and Cx45 expression in the adult regenerating skeletal muscle in response to crush injury. Within 24 h from injury, Cx37 expression was upregulated in the endothelial cells of blood vessels, and, 5 days after injury, Cx37-expressing cells were found inside the area of lesion and formed clusters generating new blood vessels with endothelial cells expressing Cx37. Three days after injury, Cx39 m…

MalePathologymedicine.medical_specialtyTime FactorsPhysiologyMuscle Fibers SkeletalConnexinNeovascularization Physiologicconnexin 45BiologyConnexinsconnexin 43Cell Fusionconnexin 40Muscle regenerationGene expressionmedicineConnexin 30MyocyteAnimalsRegenerationRNA MessengerRats WistarMuscle SkeletalIn Situ HybridizationCell AggregationCell ProliferationMyogenic cellsconnexin 39Regeneration (biology)Skeletal muscleEndothelial CellsCell Biologyconnexin 37biology.organism_classificationConstrictionImmunohistochemistryCell biologyRatsMuscle regenerationmedicine.anatomical_structureGene Expression Regulationmyogenic cellSatellite (biology)Muscle regeneration; Connexins; Myogenic cells
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