Search results for " fibrosi"

showing 10 items of 514 documents

Portrait of inflammatory response to ionizing radiation treatment

2015

Ionizing radiation (IR) activates both pro-and anti-proliferative signal pathways producing an imbalance in cell fate decision. IR is able to regulate several genes and factors involved in cell-cycle progression, survival and/or cell death, DNA repair and inflammation modulating an intracellular radiation-dependent response. Radiation therapy can modulate anti-tumour immune responses, modifying tumour and its microenvironment. In this review, we report how IR could stimulate inflammatory factors to affect cell fate via multiple pathways, describing their roles on gene expression regulation, fibrosis and invasive processes. Understanding the complex relationship between IR, inflammation and …

Ionizing radiationDNA repairFibrosimedicine.medical_treatmentClinical BiochemistryInflammationReviewCell fate determinationBioinformaticsImmune systemMedicineCytokineRegulation of gene expressionInflammationInvasivenebusiness.industryCancerIonizing radiation Inflammation Cytokine Fibrosis InvasivenessCell Biologymedicine.diseaseFibrosisInvasivenessRadiation therapyCytokineCancer researchmedicine.symptombusinessJournal of Inflammation
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Granulocyte–Macrophage Colony-Stimulating Factor Is Essential for Normal Wound Healing

2006

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a multipotent growth factor, which plays an important role during the process of wound healing. In clinical settings it has occasionally been employed in the treatment of cutaneous wounds of diverse etiologies. In a previous study, we have shown the positive influence of GM-CSF on full thickness excisional wounds in transgenic mice overexpressing GM-CSF in the basal layer of the epidermis. Direct GM-CSF action as well as indirect processes through the induction of secondary cytokines were proposed to contribute towards the beneficial effects. In this study, we analyzed the process of wound healing in transgenic mice overexpressing…

KeratinocytesMaleGenetically modified mousePathologymedicine.medical_specialtyPulmonary Fibrosismedicine.medical_treatmentNeovascularization PhysiologicMice TransgenicDermatologyNeovascularizationMiceBasal (phylogenetics)FibrosismedicineAnimalsMolecular BiologyCell ProliferationWound HealingEpidermis (botany)business.industryGrowth factorGranulocyte-Macrophage Colony-Stimulating FactorCell BiologyGeneral Medicinemedicine.diseaseGranulocyte macrophage colony-stimulating factorGranulation TissueCancer researchFemalemedicine.symptomWound healingbusinessBiotechnologymedicine.drugJournal of Investigative Dermatology Symposium Proceedings
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Oral submucous fibrosis a disease with malignant potential: report of two Cases

2010

Oral submucous fibrosis (OSF) is a high risk precancerous condition characterized by changes in the connective tissue fibers of the lamina propria and deeper parts leading to stiffness of the mucosa and restricted mouth opening. Patients with severe cases have distinct difficulties in chewing, swallowing and speaking. It predominantly occurs in Indians and other population of the Indian subcontinent with certain oral habits. In patients with submucous fibrosis, the oral epithelium becomes atrophic and thereby becomes more vulnerable to carcinogens. It is now accepted that chewing areca is the most important aetiological factor for developing OSF. The atrophic epithelium shows first an inter…

Lamina propriaPathologymedicine.medical_specialtyeducation.field_of_studybiologybusiness.industryPopulationCancerConnective tissueOdontologíamedicine.diseasebiology.organism_classification:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludPrecancerous conditionstomatognathic diseasesmedicine.anatomical_structureOral submucous fibrosisUNESCO::CIENCIAS MÉDICASCarcinomamedicineeducationbusinessGeneral DentistryAreca
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Phosphate Groups in the Lipid A Moiety Determine the Effects of LPS on Hepatic Stellate Cells: A Role for LPS-Dephosphorylating Activity in Liver Fib…

2020

Alkaline phosphatase (AP) activity is highly upregulated in plasma during liver diseases. Previously, we demonstrated that AP is able to detoxify lipopolysaccharide (LPS) by dephosphorylating its lipid A moiety. Because a role of gut-derived LPS in liver fibrogenesis has become evident, we now examined the relevance of phosphate groups in the lipid A moiety in this process. The effects of mono-phosphoryl and di-phosphoryl lipid A (MPLA and DPLA, respectively) were studied in vitro and LPS-dephosphorylating activity was studied in normal and fibrotic mouse and human livers. The effects of intestinal AP were studied in mice with CCL4-induced liver fibrosis. DPLA strongly stimulated fibrogenic…

LipopolysaccharidesLiver CirrhosisMale0301 basic medicinemedicine.medical_specialtyLipopolysaccharideNitric OxideArticleLipid AMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationInternal medicinemedicineAnimalsMacrophagePhosphorylationlipid Alcsh:QH301-705.5liver fibrosisMice Inbred BALB CInterleukin-6MacrophageslipopolysaccharideBiological activityGeneral MedicineIn vitroRatsUp-RegulationRAW 264.7 Cells030104 developmental biologyEndocrinologyLiverchemistrylcsh:Biology (General)Hepatic stellate cellAlkaline phosphatase030211 gastroenterology & hepatologylipids (amino acids peptides and proteins)hepatic stellate cellsalkaline phosphatase
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Immune Cell Toll-like Receptor 4 Mediates the Development of Obesity- and Endotoxemia-Associated Adipose Tissue Fibrosis

2014

International audience; Adipose tissue fibrosis development blocks adipocyte hypertrophy and favors ectopic lipid accumulation. Here, we show that adipose tissue fibrosis is associated with obesity and insulin resistance in humans and mice. Kinetic studies in C3H mice fed a high-fat diet show activation of macrophages and progression of fibrosis along with adipocyte metabolic dysfunction and death. Adipose tissue fibrosis is attenuated by macrophage depletion. Impairment of Toll-like receptor 4 signaling protects mice from obesity-induced fibrosis. The presence of a functional Toll-like receptor 4 on adipose tissue hematopoietic cells is necessary for the initiation of adipose tissue fibros…

LipopolysaccharidesMESH: Signal TransductionMESH: InflammationMESH : Toll-Like Receptor 4Adipose tissueMESH : AdipocytesMESH : LipopolysaccharidesMicechemistry.chemical_compoundFibrosisAdipocyteAdipocytes[ SDV.IMM ] Life Sciences [q-bio]/ImmunologyMESH: ObesityMESH: Animalslcsh:QH301-705.5Mice Inbred C3HToll-like receptorMESH : Diet High-FatMESH: Toll-Like Receptor 43. Good healthMESH: Insulin ResistanceAdipose TissueMESH: FibrosisMESH : Fibrosis[SDV.IMM]Life Sciences [q-bio]/ImmunologyMESH : ObesityMESH : Insulin ResistanceMESH: Adipose TissueSignal Transductionmedicine.medical_specialty[SDV.IMM] Life Sciences [q-bio]/ImmunologyAdipose tissue macrophagesBiologyDiet High-FatMESH : Adipose TissueGeneral Biochemistry Genetics and Molecular BiologyImmune systemMESH : Mice Inbred C3HInternal medicineMESH : MicemedicineAnimalsHumansObesityMESH: Mice Inbred C3HMESH: MiceMESH: AdipocytesInflammationMESH : Signal TransductionMESH : InflammationMESH: HumansMESH : EndotoxemiaMESH : Humans3T3-L1medicine.diseaseFibrosisMESH : Disease Models AnimalEndotoxemiaToll-Like Receptor 4Disease Models AnimalMESH: Diet High-FatEndocrinologylcsh:Biology (General)chemistryMESH: EndotoxemiaMESH : AnimalsInsulin ResistanceMESH: Disease Models AnimalMESH: LipopolysaccharidesAdipocyte hypertrophyCell Reports
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In vitro evidences of epithelial to mesenchymal transition in low cell-density cultured human fetal hepatocytes

2017

Abstract Culturing fetal hepatocytes in high cell-density allowed stabilization of the hepatocyte phenotype up to 8 weeks, including the maintenance of liver-specific functions. On the other hand, when cultured at low cell-density, fetal hepatocytes underwent morphological modifications and acquired fibroblastic morphology. Since a switch from E-cadherin to vimentin expression accompanied these changes, we hypothesized the occurrence of epithelial-to-mesenchymal transition when fetal hepatocytes were cultured at low cell-density. Changes in gene expressionsuch as up-regulation of fibrosis-related geneswere also observed, suggesting that the low cell-density culture system promoted the acqui…

Liver Cirrhosis0301 basic medicineEpithelial-Mesenchymal TransitionLiver fibrosisLiver fibrosisCell Culture TechniquesBiophysicsCell CountBiologyPrimary culturesBiochemistry03 medical and health sciencesFetal hepatocytesmedicineHumansEpithelial–mesenchymal transitionMolecular BiologyGeneCells CulturedEpithelial to mesenchymal transitionFetusTransition (genetics)Cell BiologyPhenotypeIn vitroCell biology030104 developmental biologymedicine.anatomical_structureLiverHepatocyteImmunologyHepatocytesBiochemical and Biophysical Research Communications
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Extracellular Matrix Molecular Remodeling in Human Liver Fibrosis Evolution

2016

Chronic liver damage leads to pathological accumulation of ECM proteins (liver fibrosis). Comprehensive characterization of the human ECM molecular composition is essential for gaining insights into the mechanisms of liver disease. To date, studies of ECM remodeling in human liver diseases have been hampered by the unavailability of purified ECM. Here, we developed a decellularization method to purify ECM scaffolds from human liver tissues. Histological and electron microscopy analyses demonstrated that the ECM scaffolds, devoid of plasma and cellular components, preserved the three-dimensional ECM structure and zonal distribution of ECM components. This method has been then applied on 57 l…

Liver Cirrhosis0301 basic medicineProteomicsPathologyProteomeBiopsylcsh:MedicineHepacivirusMatrix (biology)ProteomicsBiochemistryExtracellular matrixMiceLiver disease0302 clinical medicineFibrosisSettore BIO/13 - Biologia ApplicataMedicine and Health Scienceslcsh:Scienceliver fibrosisExtracellular Matrix ProteinsMultidisciplinaryDecellularizationAnimals; Extracellular Matrix; Hepacivirus; Humans; Liver; Liver Cirrhosis; Mice; Proteome; Proteomics; Tissue Scaffolds; Disease ProgressionTissue ScaffoldsChemistryLiver DiseasesLiver030220 oncology & carcinogenesisProteomeDisease ProgressionCellular Structures and OrganellesAnatomyliver fibrosis; extracellular matrix; proteomicsResearch Articlemedicine.medical_specialtyHistologySettore BIO/06extracellular matrixSurgical and Invasive Medical ProceduresGastroenterology and HepatologyScaffold03 medical and health sciencesmedicineAnimalsHumansHuman liverlcsh:RBiology and Life SciencesProteinsCell Biologymedicine.diseaseFibrosisLiver Fibrosi030104 developmental biologyLiver Fibrosis; Scaffold; Proteomicslcsh:QCollagensDevelopmental Biology
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The ABCB4 p.T175A variant as potential modulator of hepatic fibrosis in patients with chronic liver diseases: Looking beyond the cholestatic realm

2017

Liver Cirrhosis0301 basic medicinemedicine.medical_specialtyATP Binding Cassette Transporter Subfamily BCholestasisHepatologybusiness.industryABCB4Gastroenterology03 medical and health sciences030104 developmental biology0302 clinical medicineInternal medicineRealmHumansMedicine030211 gastroenterology & hepatologyIn patientbusinessHepatic fibrosisHepatology
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Is the Total Amount as Important as Localization and Type of Collagen in Liver Fibrosis Attributable to Steatohepatitis?

2020

Is liver fibrosis just liver fibrosis? Or do the subtype of collagen, its spatial localization in the liver, its cell of origin, and the time point at which it is synthesized also matter? It is important, since the various collagen subtypes hold different informative values regarding reparative processes in the liver, and as collagens have also emerged as important signaling molecules (1). Novel data have challenged our perception of liver fibrosis and collagens, which may have important implications regarding the development of new biomarkers and anti-fibrotic interventions. The traditional histological analysis of liver biopsies using histochemical collagen stains, such as the Masson's Tr…

Liver Cirrhosis0303 health sciencesPathologymedicine.medical_specialtyHepatologybusiness.industryLiver fibrosismedicine.diseaseFatty Liver03 medical and health sciences0302 clinical medicine030220 oncology & carcinogenesismedicineAnimalsHumansCollagenSteatohepatitisbusiness030304 developmental biology
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Serum ferritin is a discriminant marker for both fibrosis and inflammation in histologically proven non-alcoholic fatty liver disease patients

2011

INTRODUCTION: Differentiation between steatosis and non-alcoholic steatohepatitis (NASH) in non-alcoholic fatty liver disease (NAFLD) is important as NASH progress to cirrhosis. No specific laboratory/imaging technique exists either to diagnose NASH or to select patients for liver biopsy. PATIENTS AND METHODS: We evaluated serum ferritin and the features of metabolic syndrome with respect to histological inflammation and/or fibrosis in NAFLD patients. The Kleiner scoring system was used to classify NAFLD in consecutive liver biopsies. One hundred and eleven patients: median age 52.6, 64 males, obesity 62, diabetes mellitus (DM) 58, arterial hypertension 26 and hyperlipidaemia 40%. RESULTS: …

Liver CirrhosisAdultMaleBiopsyHyperlipidemiasFatty Liver/blood/diagnosis/etiology/pathologyRisk AssessmentSeverity of Illness IndexHepatitisBody Mass IndexDiabetes ComplicationsYoung AdultNon-alcoholic Fatty Liver DiseasePredictive Value of TestsRisk FactorsNAFLDLondonMetabolic Syndrome X/blood/*complicationsHumansAspartate AminotransferasesObesityBiological Markers/bloodliver fibrosisAgedMetabolic SyndromeInflammationFerritinChi-Square DistributionPatient SelectionNASHHepatitis/blood/complications/*diagnosisMiddle AgedFibrosisFatty LiverLiver Cirrhosis/blood/*diagnosis/etiologyNomogramsLogistic ModelsHyperlipidemias/blood/complicationsHypertension/blood/complicationsFerritinsHypertensionFerritin; Fibrosis; Inflammation; NAFLD; NASHAspartate Aminotransferases/bloodFemaleDiabetes Complications/blood/diagnosis/etiologyObesity/complicationsBiomarkersFerritins/*blood
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