Search results for "Extracellular"

showing 10 items of 1220 documents

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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Kinetics and Topology of DNA Associated with Circulating Extracellular Vesicles Released during Exercise.

2021

AbstractAlthough it is widely accepted that cancer derived extracellular vesicles (EVs) carry DNA cargo, the association of cell-free circulating DNA (cfDNA) and EVs in plasma of healthy humans remains elusive. Using a physiological exercise model, where EVs and cfDNA are synchronously released, we aimed to characterize the kinetics and localization of DNA associated with EVs. EVs were separated from human plasma using size exclusion chromatography or immuno-affinity capture for CD9+, CD63+, and CD81+ EVs. DNA was quantified with an ultra-sensitive qPCR assay targeting repetitive LINE elements, with or without DNase digestion. This model shows that a minute part of circulating cell-free DNA…

AdultMalelcsh:QH426-470KineticsexosomesExtracellular vesiclesPolymerase Chain ReactionArticle796 Athletic and outdoor sports and games570 Life sciencescell-free DNAchemistry.chemical_compoundExtracellular VesiclesYoung Adultphysical exerciseHumansExerciseCD63human plasma796 SportChemistryHealthy VolunteersCell biologylcsh:GeneticsKineticsLong Interspersed Nucleotide ElementsHuman plasmaChromatography GelCirculating DNAFemalecoronavesicular genomic DNACell-Free Nucleic AcidsDNACD81extracellular DNAintraluminal570 BiowissenschaftenGenes
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The Influence of Insulin on Local Amyloidosis of the Islets of Langerhans and Insulinoma

1980

Summary Amyloid-containing islets of Langerhans from the pancreas of 75 diabetics and one case of an amyloid-containing insulinoma were investigated. By light and electron microscopy, amyloid deposits were observed between the B cells and adjacent capillaries. The cytoplasm of B cells and extracellular amyloid display immunohistological binding of anti-insulin antibody. Correspondingly, ferritin-labeled anti-insulin antibody was found by electron microscopy on and between the amyloid fibrils. Insulin or proinsulin (or a protein closely related to insulin) thus appears to be a.component of the protein which constitutes the amyloid. The molecular weight and mode of deposition of this form of …

AdultMalemedicine.medical_specialtyAmyloidmedicine.medical_treatmentPathology and Forensic MedicineIslets of LangerhansInsulin-Secreting CellsInternal medicinemental disordersExtracellularmedicineHumansHypoglycemic AgentsInsulinInsulinomaAgedProinsulinAged 80 and overbiologyChemistryInsulinAmyloidosisAmyloidosisCell BiologyMiddle Agedmedicine.diseaseImmunohistochemistryPancreatic NeoplasmsMicroscopy Electronmedicine.anatomical_structureEndocrinologyDiabetes Mellitus Type 2biology.proteinFemaleInsulinomaAntibodyPancreasPathology - Research and Practice
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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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Plasma and fibroblasts of Tangier disease patients are disturbed in transferring phospholipids onto apolipoprotein A-I

1998

Plasmas of patients with Tangier disease (TD) lack lipid-rich α-HDL which, in normal plasma, constitutes the majority of high density lipoprotein (HDL). Residual amounts of apolipoprotein (apo)A-I in TD plasma occur as lipid-poor or even lipid-free preβ-HDL. By contrast to normal plasma, TD plasma does not convert preβ-HDL into α-HDL. Moreover, fibroblasts of TD patients were found to be defective in secreting cholesterol or phospholipids in the presence of lipid-free apoA-I. We have therefore hypothesized that both defective conversion of preβ-HDL into α-HDL and defective lipid efflux from TD cells onto lipid-free apoA-I result from a disturbance in phospholipid transfer occurring in both …

AdultMaletransferring phospholipidsPhospholipidTangier diseasePhosphatidic AcidsQD415-436PhosphatidylinositolsBiochemistrychemistry.chemical_compoundEndocrinologyTangier diseasePhosphatidylcholinePhospholipid transfer proteinExtracellularmedicineHumansCells CulturedPhosphatidylethanolamineApolipoprotein A-ICholesterolPhosphatidylethanolaminesReverse cholesterol transportnutritional and metabolic diseasesBiological TransportCell BiologyFibroblastsmedicine.diseaseMolecular biologyfamilial HDL deficiencyreverse cholesterol transportLipoproteins LDLphospholipid transfer proteinsprebeta-HDLTangier disease; transferring phospholipidschemistryPhosphatidylcholinesFemalelipids (amino acids peptides and proteins)cholesterol efflux
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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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