Search results for "Extracellular Matrix"

showing 10 items of 420 documents

Mutational screening of the USH2A gene in Spanish USH patients reveals 23 novel pathogenic mutations

2011

Abstract Background Usher Syndrome type II (USH2) is an autosomal recessive disorder, characterized by moderate to severe hearing impairment and retinitis pigmentosa (RP). Among the three genes implicated, mutations in the USH2A gene account for 74-90% of the USH2 cases. Methods To identify the genetic cause of the disease and determine the frequency of USH2A mutations in a cohort of 88 unrelated USH Spanish patients, we carried out a mutation screening of the 72 coding exons of this gene by direct sequencing. Moreover, we performed functional minigene studies for those changes that were predicted to affect splicing. Results As a result, a total of 144 DNA sequence variants were identified.…

AdultMaleSequence VariantsAdolescentGenotypegenetic structuresUsher syndromeDNA Mutational AnalysisMutation Missenselcsh:MedicineBiologymedicine.disease_causeExonYoung AdultUSH2ARetinitis pigmentosaGenotypemedicineotorhinolaryngologic diseasesHumansGenetics(clinical)Pharmacology (medical)<it>USH2A</it>GeneAllele frequencyGenetics (clinical)GeneticsMedicine(all)MutationExtracellular Matrix ProteinsResearchlcsh:RGeneral MedicineExonsMiddle Agedmedicine.diseaseeye diseasesPhenotypeSpainMutationFemalesense organsUsher SyndromeUsher SyndromesMutationsMinigeneOrphanet Journal of Rare Diseases
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MFAP5 Loss-of-Function Mutations Underscore the Involvement of Matrix Alteration in the Pathogenesis of Familial Thoracic Aortic Aneurysms and Dissec…

2014

Thoracic aortic aneurysm and dissection (TAAD) is an autosomal-dominant disorder with major life-threatening complications. The disease displays great genetic heterogeneity with some forms allelic to Marfan and Loeys-Dietz syndrome, and an important number of cases still remain unexplained at the molecular level. Through whole-exome sequencing of affected members in a large TAAD-affected family, we identified the c.472CT (p.Arg158(∗)) nonsense mutation in MFAP5 encoding the extracellular matrix component MAGP-2. This protein interacts with elastin fibers and the microfibrillar network. Mutation screening of 403 additional probands identified an additional missense mutation of MFAP5 (c.62GT …

AdultMalecongenital hereditary and neonatal diseases and abnormalitiesAdolescentExtracellular matrix componentNonsense mutationHaploinsufficiencyThoracic aortic aneurysmPathogenesisContractile ProteinsReportGeneticsmedicineHumansMissense mutationGenetics(clinical)ExomeChildGenetics (clinical)AgedGlycoproteinsAged 80 and overGeneticsAortic Aneurysm ThoracicbiologyGenetic heterogeneitySequence Analysis DNAFibroblastsMiddle Agedmedicine.diseasePedigree3. Good healthAortic DissectionAmino Acid SubstitutionCodon Nonsensebiology.proteinIntercellular Signaling Peptides and ProteinsFemaleHaploinsufficiencyElastinThe American Journal of Human Genetics
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Franceschetti Hereditary Recurrent Corneal Erosion

2011

To describe new affected individuals of Franceschetti's original pedigree of hereditary recurrent erosion and to classify a unique entity called Franceschetti corneal dystrophy.Observational case series.Slit-lamp examination of 10 affected individuals was conducted. Biomicroscopic examinations were supplemented by peripheral corneal biopsy in 1 affected patient with corneal haze. Tissue was processed for light and electron microscopy and immunohistochemistry was performed. DNA analysis was carried out in 12 affected and 3 nonaffected family members.All affected individuals suffered from severe ocular pain in the first decade of life, attributable to recurrent corneal erosions. Six adult pat…

AdultMalemedicine.medical_specialtyBiopsyDNA Mutational AnalysisDermatan SulfateCorneal dystrophyCorneal OpacityCorneal erosionAntigens NeoplasmRecurrenceTransforming Growth Factor betaOphthalmologymedicineEye PainHumansChildAgedAged 80 and overCorneal Dystrophies HereditaryExtracellular Matrix Proteinsbusiness.industryCadherinsmedicine.diseaseImmunohistochemistryPedigreeRecurrent corneal erosionOphthalmologyClaudinsFemaleDecorinbusinessCell Adhesion MoleculesChondroitinBiomarkersAmerican Journal of Ophthalmology
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Immunolocalization of Tenascin-C in Human Type II Fiber Atrophy

2000

Tenascin-C is a multifunctional extracellular matrix glycoprotein with stimulatory and anti-adhesive or inhibitory properties for axon growth. Its location and discontinuous expression are restricted in innervated muscle tissues. Tenascin-C accumulated interstitially among human denervated muscle fibers and close to normal-sized fibers. To expand our knowledge of the expression of tenascin-C in human neuromuscular disorders, we investigated immunohistologically 20 human muscle specimens with type II myofiber atrophy of children and adults. Tenascin-C immunoreactivity in adult type II atrophy was frequent, and accumulation in children was sparse and weak. In both groups, tenascin-C immunorea…

AdultMalemedicine.medical_specialtyPathologyTenascinPlatelet membrane glycoproteinExtracellular matrixCellular and Molecular NeuroscienceAtrophyInternal medicinemedicineHumansMyocyteAgedDenervationbiologyChemistryTenascin CInfantTenascinGeneral MedicineMiddle Agedmedicine.diseaseImmunohistochemistryMuscular AtrophyEndocrinologyChild PreschoolMuscle Fibers Fast-Twitchembryonic structuresbiology.proteinImmunohistochemistryFemaleJournal of Molecular Neuroscience
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Lattice Corneal Dystrophy Type 1

2014

PURPOSE To evaluate the question whether lattice corneal dystrophy type 1 (LCD1) is of epithelial or stromal origin. METHODS The landmark of advanced LCD1 shows central superficial haze and paracentral stromal lattice lines. In 16 eyes of 8 affected individuals of 2 families, a penetrating keratoplasty was performed. The follow-up was 8 to 16 years after penetrating keratoplasty. Slit-lamp documentation of the patients was evaluated in direct and indirect illumination with dilated pupil to assess the horizontal and vertical pattern of new deposits on the corneal graft. Three affected patients of 2 families are demonstrated in detail. A DNA analysis was performed. RESULTS Gene identification…

AdultMalemedicine.medical_specialtyStromal cellCorneal StromaDNA Mutational AnalysisCorneal graftCorneal KeratocytesCorneal erosionDirect illuminationTransforming Growth Factor betaOphthalmologyTGFBI genemedicineHumansCorneal Dystrophies HereditaryExtracellular Matrix Proteinsbusiness.industryEpithelium Cornealmedicine.diseaseeye diseasesOphthalmologyMutationLattice corneal dystrophyFemalebusinessKeratoplasty PenetratingTGFBICornea
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Transglutaminase Type II Plays a Protective Role in Hepatic Injury

2003

The up-regulation of "tissue" transglutaminase (TG2) gene has been shown to occur in various pathologies and can lead to severe liver injury; however, its role in the onset of liver damage has not yet been clarified. To address this issue, we have used two experimental settings: carbon tetrachloride (CCl(4))-induced liver injury in wild-type and TG2 knockout mice; and liver biopsies obtained from a large cohort of hepatitis C virus (HCV)-infected patients. Mice lacking TG2 failed to clear the hepatic necrotic tissue formed in response to prolonged CCl(4) exposure (5 weeks) and 60% of them died before the end of the treatment. By contrast, wild-type mice were able to recover after the toxic …

AdultPathologymedicine.medical_specialtyNecrosisGenotypeTissue transglutaminaseHepatitis C virusCCL4medicine.disease_causeGene Expression Regulation EnzymologicPathology and Forensic MedicineExtracellular matrixMiceNecrosisGTP-Binding ProteinsmedicineAnimalsHumansProtein Glutamine gamma Glutamyltransferase 2Mice KnockoutHepatitisLiver injuryTransglutaminasesbiologyCarbon Tetrachloride PoisoningHepatitis C ChronicMiddle Agedmedicine.diseaseMice Inbred C57BLLiverKnockout mousebiology.proteinmedicine.symptomRegular ArticlesThe American Journal of Pathology
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A novel mutation of the extracellular matrix protein 1 gene (ECM1) in a patient with lipoid proteinosis (Urbach-Wiethe disease) from Sicily

2005

Summary Background  Lipoid proteinosis (LP), also known as Urbach–Wiethe disease, is a rare autosomal recessive disorder characterized by a hoarse voice, warty skin infiltration and scarring. Mutations within the extracellular matrix protein 1 (ECM1) gene cause LP. Objectives  We report the molecular analysis of the ECM1 gene in a Sicilian patient with LP in order to extend the mutation spectrum of this genodermatosis. Methods  We studied a 32-year-old female born from consanguineous parents who was diagnosed at the age of 11 years as having LP. She has a clinical phenotype corresponding to Urbach–Wiethe disease characterized by papules/nodules, indurated plaques and sometimes ulcerated les…

AdultPathologymedicine.medical_specialtySettore MED/09 - Medicina InternaBiopsyMolecular Sequence DataNonsense mutationDermatologyBiologyUrbach–Wiethe diseasemedicine.disease_causePolymerase Chain ReactionFrameshift mutationExtracellular matrix protein 1ExonmedicineHumanseducationSicilyGeneExtracellular Matrix Proteinseducation.field_of_studyMutationBase SequenceGenodermatosisSkin Diseases Geneticmedicine.diseasePedigreeECM1 gene lipoid proteinosis mutationSettore MED/03 - Genetica MedicaCodon NonsenseLipoid Proteinosis of Urbach and WietheSettore MED/26 - NeurologiaFemaleBritish Journal of Dermatology
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Adhesive and invasive features in gliomas

2000

Summary This study aims at the in situ identification of factors mediating glioma cell invasion requiring adhesion, extracellular matrix degradation, and migration. Fortyfive gliomas (astrocytomas, glioblastomas, oligodendrogliomas, and mixed gliomas) were investigated for the immunohistochemical expression of the membrane protein CD44s, the basal lamina proteins laminin, collagen IV, and fibronectin, the lectin galectin-3 recognizing tenascin and N-CAM, as well as for the matrix-degrading enzymes metalloproteinases MMP-2, MMP-9, and cathepsin D. Besides vessels expressing basal lamina proteins, tenascin, MMP-2, MMP-9, and galectin-3, tumor cells revealed strong immunoreactivity for CD44s, …

AdultPathologymedicine.medical_specialtyanimal structuresTenascinPathology and Forensic MedicineExtracellular matrixReference ValuesLamininCell AdhesionmedicineHumansNeoplasm InvasivenessCell adhesionAgedAged 80 and overCathepsinExtracellular Matrix ProteinsbiologyBrain NeoplasmsTenascin CBrainGliomaCell BiologyMiddle AgedFibronectinmedicine.anatomical_structurebiology.proteinCancer researchBasal laminaPathology - Research and Practice
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Sputum metalloproteinase-9/tissue inhibitor of metalloproteinase-1 ratio correlates with airflow obstruction in asthma and chronic bronchitis

1998

Asthma and chronic bronchitis are inflammatory diseases with extracellular matrix (ECM) remodeling and collagen deposition. Collagen homeostasis is controlled by metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs). We evaluated MMP and TIMP balance in induced sputum of 10 control, 31 untreated asthmatic, and 16 chronic bronchitic subjects. We first performed zymographic analysis to identify the profile of MMPs. Zymography revealed a similar MMPs profile in all populations studied and that MMP-9 was the major enzyme released. We then measured, using enzyme immunoassay, the concentrations of MMP-9 and of its inhibitor TIMP-1 and evaluated whether airflow limitation m…

AdultPulmonary and Respiratory MedicineChronic bronchitisAdolescentNeutrophilsCell CountEnzyme-Linked Immunosorbent AssayMatrix metalloproteinaseCritical Care and Intensive Care MedicinePathogenesisLeukocyte CountSurface-Active AgentsForced Expiratory VolumemedicineHomeostasisHumansProtease InhibitorsCollagenasesBronchitisAgedAsthmaTissue Inhibitor of Metalloproteinase-1business.industryMacrophagesRespiratory diseaseSputumSodium Dodecyl SulfateMiddle AgedTissue inhibitor of metalloproteinasemedicine.diseaseAsthmaExtracellular Matrixrespiratory tract diseasesAirway ObstructionMatrix Metalloproteinase 9Chronic DiseaseImmunologyBronchitisSputumElectrophoresis Polyacrylamide GelCollagenmedicine.symptomPulmonary Ventilationbusiness
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YAP/TAZ activity in stromal cells prevents ageing by controlling cGAS-STING

2022

Ageing is intimately connected to the induction of cell senescence(1,2), but why this is so remains poorly understood. A key challenge isthe identification of pathways that normally suppress senescence, are lost during ageing and are functionally relevant to oppose ageing(3). Here we connected the structural and functional decline of ageing tissues to attenuated function of the master effectors of cellular mechanosignalling YAP and TAZ. YAP/TAZ activity declines during physiological ageing in stromal cells, and mimicking such decline through genetic inactivation of YAP/TAZ in these cells leads to accelerated ageing. Conversely, sustaining YAP function rejuvenates old cells and opposes the e…

AgingMechanotransductionActin-Related Protein 2; Cellular Senescence; Extracellular Matrix; Healthy Aging; Immunity Innate; Lamin Type B; Mechanotransduction Cellular; Nuclear Envelope; Signal Transduction; Aging; Membrane Proteins; Nucleotidyltransferases; Stromal Cells; Transcriptional Coactivator with PDZ-Binding Motif Proteins; YAP-Signaling ProteinsNuclear EnvelopeSettore MED/08 - Anatomia PatologicaYAP TAZ ageing C-GAS STINGMechanotransduction CellularArticleHealthy AgingInnateCellular SenescenceAdaptor Proteins Signal TransducingMultidisciplinaryLamin Type BImmunityMembrane ProteinsYAP-Signaling ProteinsPhosphoproteinsNucleotidyltransferasesImmunity InnateExtracellular MatrixTranscriptional Coactivator with PDZ-Binding Motif ProteinsActin-Related Protein 2CellularStromal CellsSignal Transduction
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