Search results for "Acellular"

showing 10 items of 1986 documents

Increased hepatic fibrosis and JNK2-dependent liver injury in mice exhibiting hepatocyte-specific deletion of cFLIP.

2012

Chronic liver disease promotes hepatocellular injury involving apoptosis and triggers compensatory regeneration that leads to the activation of quiescent stellate cells in the liver. The deposition of extracellular matrix from activated myofibroblasts promotes hepatic fibrosis and the progression to cirrhosis with deleterious effects on liver physiology. The role of apoptosis signaling pathways in the development of fibrosis remains undefined. The aim of the current study was to determine the involvement of the caspase-8 homologue cellular FLICE-inhibitory protein (cFLIP) during the initiation and progression of fibrosis. Liver injury and fibrosis from carbon tetrachloride (CCl4) and thioa…

Liver CirrhosisMalePathologymedicine.medical_specialtyTime FactorsGenotypePhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinApoptosisBiologyThioacetamideChronic liver diseaseMicePhysiology (medical)medicineAnimalsMitogen-Activated Protein Kinase 9PhosphorylationExtracellular Signal-Regulated MAP KinasesCarbon TetrachlorideCompensatory regenerationLiver injuryMice KnockoutHepatologyCaspase 3Gastroenterologymedicine.diseaseCaspase 9Enzyme ActivationDisease Models Animalmedicine.anatomical_structurePhenotypeLiverApoptosisHepatocyteHepatic stellate cellCancer researchDisease ProgressionHepatocytesHepatocellular injuryChemical and Drug Induced Liver InjuryHepatic fibrosisSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
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Serum coding and non-coding RNAs as biomarkers of NAFLD and fibrosis severity

2019

Background & Aims: In patients with non-alcoholic fatty liver disease (NAFLD), liver biopsy is the gold standard to detect non-alcoholic steatohepatitis (NASH) and stage liver fibrosis. We aimed to identify differentially expressed mRNAs and non-coding RNAs in serum samples of biopsy-diagnosed mild and severe NAFLD patients with respect to controls and to each other. Methods: We first performed a whole transcriptome analysis through microarray (n = 12: four Control: CTRL; four mild NAFLD: NAS ≤ 4 F0; four severe NAFLD NAS ≥ 5 F3), followed by validation of selected transcripts through real-time PCRs in an independent internal cohort of 88 subjects (63 NAFLD, 25 CTRL) and in an external …

Liver CirrhosisMaleRNA UntranslatedMicroarrayBiopsyGastroenterologyliquid-biopsySeverity of Illness IndexTranscriptomeCohort Studies0302 clinical medicineFibrosisSettore BIO/13 - Biologia ApplicataNon-alcoholic Fatty Liver DiseaseMedicineSettore MED/12 - Gastroenterologiamedicine.diagnostic_testFatty liverArea under the curveNASHUntranslatedMiddle AgedLiver030220 oncology & carcinogenesisLiver biopsyDisease Progression030211 gastroenterology & hepatologyFemalefibrosiAdultmedicine.medical_specialty03 medical and health sciencesPredictive Value of TestsInternal medicineNAFLDliquid‐biopsyExtracellularHumansHepatologybusiness.industryGene Expression Profilingfibrosismedicine.diseaseRNAsMetabolic Liver DiseaseROC CurveRNASteatohepatitisbusinessBiomarkers
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StellaTUM: current consensus and discussion on pancreatic stellate cell research

2011

The field of pancreatic stellate cell (PSC) biology is very young, as the essential in-vitro tools to study these cells (ie, methods to isolate and culture PSC) were only developed as recently as in 1998. Nonetheless, there has been an exponential increase in research output in this field over the past decade, with numerous research groups around the world focusing their energies into elucidating the biology and function of these cells. It is now well established that PSC are responsible for producing the stromal reaction (fibrosis) of two major diseases of the pancreas—chronic pancreatitis and pancreatic cancer. Despite exponentially increasing data, the methods for studying PSC remain var…

Liver CirrhosisPathologycell migrationpancreatic cancerCellpancreatitisPancreatic stellate cellLeading Articlehepatic surgerycell biologymolecular biologyhepatic fibrosis1506pancreaspancreatic surgerysignallinghepatic stellate cellalcoholPancreatic Stellate CellsGastroenterologypancreatic functionddc:medicine.anatomical_structurePancreaspancreatic fibrosissignal transductionstellate cellsmedicine.medical_specialtyStromal cellacute pancreatitisextracellular matrixadjuvant treatmentAbdominal surgerycancer geneticsliverpancreatic enzymesdigestive systemchronic pancreatitisstem cellsPancreatitis ChronicPancreatic cancermedicinecancerHumansRegenerationpancreatic physiologyendoscopyProgenitor cellmarkeradenocarcinomaHelicobacter pyloribusiness.industryfibrosisPancreatic Diseasesmedicine.diseaseexperimental pancreatitisLiver RegenerationPancreatic Neoplasmspancreatic pathologyconsensusCancer cellgene expressionHepatic stellate cellbusinesspancreatic diseaseGut
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Tissue transglutaminase in HCV infection.

2003

Liver CirrhosisTransglutaminasesbiologybusiness.industryTissue transglutaminaseCell BiologyFibrosisHepatitis CGTP-Binding Proteinsbiology.proteinCancer researchHepatocytesMedicineHumansProtein Glutamine gamma Glutamyltransferase 2businessExtracellular SpaceMolecular BiologyCell death and differentiation
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Liver fibrosis induced by hepatic overexpression of PDGF-B in transgenic mice

2006

Background/Aims In hepatic fibrogenesis, stellate cells are activated leading to production and deposition of extracellular matrix. To clarify the role of PDGF-B in liver fibrogenesis, we overexpressed PDGF-B in the liver of transgenic mice. Methods Transgenic mice for the conditional overexpression of PDGF-B in the liver under control of an albumin promoter were generated utilising the Cre/loxP system. Constitutive PDGF-B expression was achieved after breeding with mice expressing Cre-recombinase under actin promoter control. Tamoxifen inducible expression was achieved after breeding with mice expressing Cre under transthyretin receptor promoter control. Levels of fibrosis were assessed an…

Liver Cirrhosismedicine.medical_specialtyPlatelet-derived growth factorLiver cytologyTransgeneMice TransgenicBiologyMicechemistry.chemical_compoundTransforming Growth Factor betaFibrosisInternal medicinemedicineAnimalsPromoter Regions GeneticCells CulturedCell ProliferationIntegrasesHepatologyTransdifferentiationCell DifferentiationProto-Oncogene Proteins c-sisFibroblastsmedicine.diseaseExtracellular MatrixEndocrinologyGene Expression RegulationLiverchemistryHepatocytesCancer researchHepatic stellate cellHepatic fibrosisMyofibroblastJournal of Hepatology
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Colorectal cancer-derived small extracellular vesicles induce TGFβ1-mediated epithelial to mesenchymal transition of normal hepatocytes: new insights…

2023

More than 50% of patients affected by colorectal cancer (CRC) present liver metastasis, which is the most frequent cause of CRC-associated death. Numerous studies have shown that metastatic cascade is the result of complex mechanisms based on two-way interactions between invasive CRC cells and liver resident cells. In recent years, several findings have demonstrated that small extracellular vesicles (SEVs) released by cancer cells play a crucial role in the formation of pre-metastatic niche in the liver, specifically affecting the activities of non-parenchymal cells as Kupffer cells and hepatic stellate cells. However, although hepatocytes (heps) are the most conspicuous in the liver, their…

Liver metastasiTransforming growth factor‑β1 (TGFβ1).Small extracellular vesicleHepatocyteColorectal cancer
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Cellular Oxygen Concentration

1976

At low oxygen levels the intracellular or intramitochondrial concentration of molecular oxygen together with the amount of reduced cytochrome oxydase determines the rate of oxygen utilization. Below the so-called “critical oxygen concentration”, i.e. the value, at which a drop in the rate of oxygen uptake has its first evidence, the kinetic is described by the oxygen affinity (Km) of the respiratory chain, i.e. the concentration value for half maximal rate of oxygen uptake.

Low oxygenCytochromebiologyChemistryCellular oxygenBiophysicsApparent oxygen utilisationRespiratory chainbiology.proteinLimiting oxygen concentrationPartial pressureIntracellular
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Stx5 is a novel interactor of VLDL-R to affect its intracellular trafficking and processing

2012

We identified syntaxin 5 (Stx5), a protein involved in intracellular vesicle trafficking, as a novel interaction partner of the very low density lipoprotein (VLDL)-receptor (VLDL-R), a member of the LDL-receptor family. In addition, we investigated the effect of Stx5 on VLDL-R maturation, trafficking and processing. Here, we demonstrated mutual association of both proteins using several in vitro approaches. Furthermore, we detected a special maturation phenotype of VLDL-R resulting from Stx5 overexpression. We found that Stx5 prevented advanced Golgi-maturation of VLDL-R, but did not cause accumulation of the immature protein in ER, ER to Golgi compartments, or cis-Golgi ribbon, the main ex…

Low-density lipoprotein receptor-related protein 8Very Low-Density Lipoprotein ReceptorCHO CellsSTX5Biologysymbols.namesakeCricetulusCricetinaeAnimalsHumansSyntaxinSecretory PathwayQa-SNARE ProteinsCell Membranenutritional and metabolic diseasesIntracellular vesicleHep G2 CellsCell BiologyGolgi apparatusCell biologyProtein TransportHEK293 CellsReceptors LDLLDL receptorsymbolslipids (amino acids peptides and proteins)Protein Processing Post-TranslationalIntracellularProtein Bindingtrans-Golgi NetworkExperimental Cell Research
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Pyramidal and nonpyramidal callosal cells in the striate cortex of the adult rat

1994

The aim of this study has been to determine the neuronal types (pyramidal and nonpyramidal) within the rat's visual cortex, which project through the corpus callosum. To this end, the morphology and laminar distribution of callosal cells have been investigated by combining Diamidino Yellow retrograde tracing with intracellular injection of Lucifer Yellow in slightly fixed tissue slices. The visual callosal projection arises from pyramidal cells of diverse morphology in layers II to VIb, as well as from several modified pyramids located mainly in layers II, IV (star pyramids) and VIb (horizontal or inverted pyramids and related forms of spiny stellate cells). Our results indicate that in rat…

Lucifer yellowGeneral NeuroscienceAnatomyBiologyCorpus callosumRetrograde tracingMultipolar neuronchemistry.chemical_compoundmedicine.anatomical_structureVisual cortexnervous systemchemistrymedicineHepatic stellate cellAxoplasmic transportNeuroscienceIntracellularJournal of Comparative Neurology
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Sphingosine-1-phosphate increases human alveolar epithelial IL-8 secretion, proliferation and neutrophil chemotaxis

2009

Sphingosine-1-phosphate (S1P) has been presented recently as a pro-inflammatory agent in the airway epithelium since S1P levels are increased in bronchoalveolar lavage fluid of human asthmatics. However, the effects of S1P over the alveolar epithelium and neutrophil interactions are poorly understood. Here, we show that S1P increased interleukin 8 (IL-8) gene expression and protein secretion and proliferation in alveolar epithelial cells A549 at physiological concentrations (1 microM). At the same time, S1P increased intracellular Ca2+ concentration (potency 17.91 microM, measured by epifluorescence microscopy), phospholipase D (PLD) activity (measured by chemiluminiscence method) and extra…

LuminescenceNeutrophilsIntercellular Adhesion Molecule-1Gene ExpressionBiologyPertussis toxinReceptors G-Protein-Coupled1-ButanolSphingosineCell Line TumorPhospholipase DHumansInterleukin 8PhosphorylationExtracellular Signal-Regulated MAP KinasesEgtazic AcidCell ProliferationFlavonoidsPharmacologyA549 cellCell adhesion moleculeInterleukin-8Epithelial CellsChemotaxisIntercellular Adhesion Molecule-1Intercellular adhesion moleculeMolecular biologyPulmonary AlveoliChemotaxis LeukocytePertussis ToxinBiochemistryRespiratory epitheliumCalciumlipids (amino acids peptides and proteins)LysophospholipidsEuropean Journal of Pharmacology
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