Search results for " Connexin"

showing 8 items of 8 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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Influence of genetic polymorphisms and mutations in the cardiac pathology of iron overload in thalassemia and sickle cell anemia patients: a retrospe…

2012

Cardiac disease in thalassemia is determined by the accumulation of iron in the tissue. Genetic factors could influence the severity and the rapidity of the modifications of the cardiac tissue. Mutations or polymorphisms of genes have already been described as being implicated in cardiac disease. In particular, we studied the polymorphisms C1091T in the Connexin 37 gene (CX 37), 4G -668 5G in the Plasminogen Activator Inhibitor-1 gene (PAI 1) and 5A-1171 6A in the Stromelysin-1 gene (SL) in 193 randomly selected patients affected by hemoglobinopathies and 100 normal subjects randomly selected from the general population. A retrospective analysis based on history, clinical data and imaging s…

medicine.medical_specialtyPathologyHeart diseasebusiness.industryThalassemiaCardiac pathologyRetrospective cohort studymedicine.diseaseGastroenterologySickle cell anemiaInternal medicinemedicineDiseases of the blood and blood-forming organsRC633-647.5businessheart disease PAI-1 Stromelysin Connexin 37.heart disease PAI-1 stromelysin connexin 37.heart disease; PAI-1; stromelysin; connexin 37Thalassemia Reports
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Connexin36 (Cx36) expression and protein detection in the mouse carotid body and myenteric plexus

2013

AbstractAlthough connexin36 (Cx36) has been studied in several tissues, it is notable that no data are available on Cx36 expression in the carotid body and the intestine. The present study was undertaken to evaluate using immunohistochemistry, PCR and Western blotting procedures, whether Cx36 was expressed in the mouse carotid body and in the intestine at ileum and colon level. In the carotid body, Cx36 was detected as diffuse punctate immunostaining and as protein by Western blotting and mRNA by RT-PCR. Cx36 punctate immunostaining was also evident in the intestine with localization restricted to the myenteric plexus of both the ileum and the colon, and this detection was also confirmed by…

MalePathologymedicine.medical_specialtyHistologyMousegenetic structuresMyenteric plexusBlotting WesternIleumConnexinBiologySettore BIO/09 - FisiologiaConnexinsMice03 medical and health sciences0302 clinical medicinemedicineAnimalsGap junctionsMyenteric plexus030304 developmental biologyMice Knockout0303 health sciencesReverse Transcriptase Polymerase Chain ReactionGap junctions Carotid body Myenteric plexus Connexin Cx36 MouseCell BiologyGeneral MedicineImmunohistochemistryMolecular biologyMice Inbred C57BLBlotCarotid bodymedicine.anatomical_structureReal-time polymerase chain reactionCx36Knockout mouseImmunohistochemistryCarotid bodysense organs030217 neurology & neurosurgeryImmunostaining
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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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Identification of D179H, a novel missense GJB2 mutation in a Western Sicily family

2013

The main purpose of this study was to describe a novel missense mutation (p.D179H) found in a Western Sicily family and to examine the genetic and audiologic profiles of all family members by performing a GJB2 and GJB6 mutations analysis and a complete audiologic assessment. The proband was a 3-month-old infant with a congenital profound sensorineural hearing loss; direct sequencing of the GJB2 revealed the presence of a c.35delG mutation in the heterozygous state and a heterozygous G[C transition at nucleotide 535 in trans; this novel mutation, called p.D179H, resulted in an aspartic acid to histidine change at codon 179. It was also evidenced in the heterozygous state in two members of th…

AdultProbandNovel mutationGenotypeHearing Loss SensorineuralDNA Mutational AnalysisNonsense mutationMutation MissenseGenes RecessiveCongenital hearing lossConnexin mutationSeverity of Illness IndexConnexinsmedicineHumansMissense mutationFamilySicilyGeneticsbiologyTransition (genetics)InfantGeneral Medicinemedicine.diseaseGJB2Settore MED/32 - AudiologiaPedigreeNovel mutation Connexin mutation GJB2Sensorineural hearing loss Congenital hearing lossConnexin 26Settore MED/31 - OtorinolaringoiatriaNovel mutation; Connexin mutation; GJB2OtorhinolaryngologyMutation (genetic algorithm)biology.proteinSettore MED/26 - NeurologiaSensorineural hearing lossGJB6European Archives of Oto-Rhino-Laryngology
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Recovery of Damaged Skeletal Muscle in mdx Mice through Low-intensity Endurance Exercise

2013

The lack of dystrophin in mdx mice leads to cycles of muscle degeneration and regeneration processes. Various strategies have been proposed in order to reduce the muscle-wasting component of muscular dystrophy, including implementation of an exercise programme. The aim of this study was to examine how low-intensity endurance exercise affects the degeneration-regeneration process in dystrophic muscle of male mdx mice. Mice were subjected to low-intensity endurance exercise by running on a motorized Rota-Rod for 5 days/week for 6 weeks. Histomorphological analysis showed a signifi cant reduction of measured inflammatory-necrotic areas in both gastrocnemius and quadriceps muscle of exercised m…

Malemusculoskeletal diseasesmedicine.medical_specialtyBlotting WesternConnexinPhysical Therapy Sports Therapy and RehabilitationDegeneration (medical)Settore BIO/09 - FisiologiaConnexinsMiceRandom Allocationdystrophic muscle muscle regeneration muscle injury connexin connexin 39 muscle strengthEndurance trainingPhysical Conditioning AnimalInternal medicinemedicineAnimalsRegenerationOrthopedics and Sports MedicineMuscle StrengthMuscular dystrophyMuscle SkeletalbiologyMuscle fatiguebusiness.industrySkeletal muscleAnatomyMuscular Dystrophy Animalmedicine.diseaseExercise TherapyMice Inbred C57BLmedicine.anatomical_structureEndocrinologyMuscle FatigueMice Inbred mdxPhysical Endurancebiology.proteinmedicine.symptomDystrophinbusinessBiomarkersMuscle ContractionMuscle contraction
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A novel DFNB1 deletion allele supports the existence of a distant cis-regulatory region that controls GJB2 and GJB6 expression

2010

Contains fulltext : 87760_1.pdf (author's version ) (Open Access) Contains fulltext : 87760_2.pdf (Publisher’s version ) (Closed access) Eleven affected members of a large German-American family segregating recessively inherited, congenital, non-syndromic sensorineural hearing loss (SNHL) were found to be homozygous for the common 35delG mutation of GJB2, the gene encoding the gap junction protein Connexin 26. Surprisingly, four additional family members with bilateral profound SNHL carried only a single 35delG mutation. Previously, we demonstrated reduced expression of both GJB2 and GJB6 mRNA from the allele carried in trans with that bearing the 35delG mutation in these four persons. Usin…

MaleGenetics and epigenetic pathways of disease [NCMLS 6][SDV]Life Sciences [q-bio]PenetranceMESH: Base SequenceRegulatory Sequences Nucleic Acidsensorineural hearing lossConnexinsMESH: GenotypeMESH: Hearing Loss Sensorineural/diagnosisMESH: PenetranceGenotypeCopy-number variationGenetics (clinical)Sequence DeletionGeneticsComparative Genomic Hybridization0303 health sciencesMESH: Genetic TestingMESH: Gene Expression Regulation*030305 genetics & heredityPenetranceGJB2PedigreeConnexin 26MESH: Sequence Deletion*MESH: Hearing Loss Sensorineural/geneticsFemaleChromosome DeletionFunctional Neurogenomics [DCN 2]GJB6GenotypeMESH: PedigreeMESH: Chromosome DeletionHearing Loss SensorineuralMolecular Sequence Dataconnexin 26connexin 30DFNB1gene expression regulationGJB2GJB6sensorineural hearing losssequence deletionBiologyMESH: Connexin 30MESH: Connexins/genetics*MESH: Sequence Homology Nucleic AcidArticleGenomic disorders and inherited multi-system disorders [IGMD 3]03 medical and health sciencesMonoallelic MutationGJB6MESH: Connexin 26Sequence Homology Nucleic AcidConnexin 30otorhinolaryngologic diseasesGeneticsHumansGenetic TestingAlleleGeneMESH: Regulatory Sequences Nucleic Acid/genetics*AllelesDFNB1030304 developmental biologyFamily HealthMESH: HumansMESH: Molecular Sequence DataBase SequenceChromosomes Human Pair 13MESH: AllelesBreakpointMESH: MaleMESH: Comparative Genomic HybridizationGene Expression RegulationMESH: Family Healthbiology.proteinHuman medicineMESH: Chromosomes Human Pair 13/geneticsMESH: FemaleClinical Genetics
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Antiabsence effects of carbenoxolone in two genetic animal models of absence epilepsy (WAG/Rij rats and lh/lh mice).

2005

Carbenoxolone (CBX), the succinyl ester of glycyrrhetinic acid, is an inhibitor of gap junctional intercellular communication. We have tested its possible effects upon two genetic animal models of epilepsy (WAG/Rij rats and lethargic (lh/lh) mice). Systemic administration of CBX was unable to significantly affect the occurrence of absence seizures in WAG/Rij rats. In particular, intravenous (5-40 mg/kg) or intraperitoneal (i.p.; 10-80 mg/kg) administration of CBX was unable to significantly modify the number and duration of spike-wave discharges (SWDs) in WAG/Rij rats, whereas the bilateral microinjection (0.05, 0.1, 0.5 and 1 microg/0.5 microl) of CBX into nucleus reticularis thalami (NRT)…

Malemedicine.medical_specialtyTime FactorsCarbenoxoloneConnexinConnexinsCellular and Molecular Neurosciencechemistry.chemical_compoundEpilepsyMiceMice Neurologic MutantsInternal medicinemedicineAnimalsGlycyrrhizinMicroinjectionGap junctionsPharmacologyDose-Response Relationship DrugGap junctionElectroencephalographyRats Inbred StrainsEpilepsy Carbenoxolone WAG/Rij rat Lethargic mouse Gap junction Connexin Absence seizuresmedicine.diseaseRatsDisease Models AnimalEndocrinologymedicine.anatomical_structurechemistryEpilepsy AbsenceGene Expression RegulationThalamic NucleiSystemic administrationCarbenoxoloneepilepsyAutoradiographyNucleusmedicine.drugGap junctions; Carbenoxolone ; epilepsyNeuropharmacology
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