Search results for " Cell"

showing 10 items of 14074 documents

Ovarian Transcriptomic Analysis Reveals Differential Expression Genes Associated with Cell Death Process after Selection for Ovulation Rate in Rabbits

2020

[EN] Transcriptomic analysis showed nineteen potential biomarkers in ovarian tissue from females belonged to a rabbit line selected for ovulation rate for 10 generations and the control line. These females differed not only in ovulation rate but also in prenatal survival since similar litter size were observed. Litter size is an essential trait in rabbit meat production but with low heritability. A selection experiment for ovulation rate has been performed for 10 generations to improve litter size in rabbits. The selected line increased two ova more than the control line but nevertheless a negative correlation was observed with prenatal survival. A transcriptomic study was performed, using …

0301 basic medicineLitter (animal)Programmed cell deathmedia_common.quotation_subjectRabbitPRODUCCION ANIMALBiologyTranscriptomic analysisArticleAndrologyTranscriptome03 medical and health sciences0302 clinical medicineControl lineOvulation ratelcsh:Zoologylcsh:QL1-991OvulationGenemedia_commonlcsh:Veterinary medicine030219 obstetrics & reproductive medicineGeneral VeterinaryOvarian tissueHeritabilityGENETICALitter size030104 developmental biologyCell Death Processlcsh:SF600-1100Animal Science and ZoologyAnimals
researchProduct

Determinants of fibrosis progression and regression in NASH

2017

Cirrhosis has become the major liver-related clinical endpoint in non-alcoholic steatohepatitis (NASH). However, progression to cirrhosis is less predictable in NASH than in other chronic liver diseases. This is due to the complex and multifactorial aetiology of NASH, which is determined by lifestyle and nutrition, multiple genetic and epigenetic factors, and a prominent role of hepatic and extrahepatic comorbidities. Thus, modest changes in these cofactors can also induce fibrosis regression, at least in patients with precirrhotic liver disease. Fibrogenesis in NASH correlates with, but is indirectly coupled to, classical inflammation, since fibrosis progression is driven by repetitive per…

0301 basic medicineLiver CirrhosisCirrhosisInflammationBioinformaticsCholangiocyte03 medical and health sciencesLiver disease0302 clinical medicineFibrosisNon-alcoholic Fatty Liver DiseaseClinical endpointMedicineHumansHepatologybusiness.industryDisease Managementmedicine.diseasePrognosis3. Good health030104 developmental biologyImmunologyHepatic stellate cellDisease Progression030211 gastroenterology & hepatologySteatohepatitismedicine.symptombusinessJournal of Hepatology
researchProduct

Hepatocyte pyroptosis and release of inflammasome particles induce stellate cell activation and liver fibrosis.

2019

Background & Aims Increased hepatocyte death contributes to the pathology of acute and chronic liver diseases. However, the role of hepatocyte pyroptosis and extracellular inflammasome release in liver disease is unknown. Methods We used primary mouse and human hepatocytes, hepatocyte-specific leucine 351 to proline Nlrp3KICreA mice, and GsdmdKO mice to investigate pyroptotic cell death in hepatocytes and its impact on liver inflammation and damage. Extracellular NOD-, LRR-, and pyrin domain-containing protein 3 (NLRP3) inflammasomes were isolated from mutant NLRP3-YFP HEK cells and internalisation was studied in LX2 and primary human hepatic stellate cells. We also examined a cohort of 154…

0301 basic medicineLiver CirrhosisInflammasomesInterleukin-1betaArticle03 medical and health sciencesLiver diseaseMice0302 clinical medicineMice Inbred NODNon-alcoholic Fatty Liver DiseaseNLR Family Pyrin Domain-Containing 3 ProteinmedicineHepatic Stellate CellsPyroptosisAnimalsHumansLiver injuryHepatologyChemistryFatty liverCaspase 1PyroptosisInflammasomemedicine.disease3. Good healthCell biology030104 developmental biologymedicine.anatomical_structureHepatocyteHepatic stellate cellHepatocytesProtein Translocation Systems030211 gastroenterology & hepatologySteatohepatitisReactive Oxygen Speciesmedicine.drugJournal of hepatology
researchProduct

Nuclear Translocation of RELB Is Increased in Diseased Human Liver and Promotes Ductular Reaction and Biliary Fibrosis in Mice.

2019

Background & Aims Cholangiocyte proliferation and ductular reaction contribute to the onset and progression of liver diseases. Little is known about the role of the transcription factor nuclear factor-κB (NF-κB) in this process. We investigated the activities of the RELB proto-oncogene NF-κB subunit in human cholangiocytes and in mouse models of liver disease characterized by a ductular reaction. Methods We obtained liver tissue samples from patients with primary sclerosing cholangitis, primary biliary cholangitis, hepatitis B or C virus infection, autoimmune hepatitis, alcoholic liver disease, or without these diseases (controls) from a tissue bank in Germany. Tissues were analyzed by immu…

0301 basic medicineLiver CirrhosisMaleAlcoholic liver diseaseCholangiocyte proliferationAutoimmune hepatitisProto-Oncogene MasLiver diseaseMice0302 clinical medicineCarbon TetrachlorideCells CulturedRELBLiver DiseasesGastroenterologyMiddle Aged3. Good healthDeubiquitinating Enzyme CYLDCysteine EndopeptidasesProtein TransportLiverGene Knockdown TechniquesCytokines030211 gastroenterology & hepatologyFemaleCell activationAdultLymphotoxin-betaAdolescentCholangitis SclerosingPrimary sclerosing cholangitis03 medical and health sciencesYoung AdultLymphotoxin beta ReceptormedicineAnimalsHumansRNA MessengerParenchymal TissueAgedCell ProliferationCell NucleusHepatologybusiness.industryTranscription Factor RelBEpithelial CellsDicarbethoxydihydrocollidinemedicine.diseaseFibrosis030104 developmental biologyCancer researchLiver functionBile DuctsbusinessGastroenterology
researchProduct

Protein tyrosine phosphatase 1b deficiency protects against hepatic fibrosis by modulating nadph oxidases

2019

Inflammation is typically associated with the development of fibrosis, cirrhosis and hepatocellular carcinoma. The key role of protein tyrosine phosphatase 1B (PTP1B) in inflammatory responses has focused this study in understanding its implication in liver fibrosis. Here we show that hepatic PTP1B mRNA expression increased after bile duct ligation (BDL), while BDL-induced liver fibrosis was markedly reduced in mice lacking Ptpn1 (PTP1B−/−) as assessed by decreased collagen deposition and α-smooth muscle actin (α-SMA) expression. PTP1B−/− mice also showed a significant increase in mRNA levels of key markers of monocytes recruitment (Cd68, Adgre1 and Ccl2) compared to their wild-type (PTP1B+…

0301 basic medicineLiver CirrhosisMaleClinical BiochemistryGene ExpressionApoptosisBiochemistryMice0302 clinical medicineFibrosisTransforming Growth Factor betaRNA Small Interferinglcsh:QH301-705.5Liver injuryProtein Tyrosine Phosphatase Non-Receptor Type 1lcsh:R5-920NADPH oxidaseProtein tyrosine phosphatase 1BbiologyChemistryNOX4Bile duct ligationImmunohistochemistry3. Good healthNOX1Femalelcsh:Medicine (General)hormones hormone substitutes and hormone antagonistsResearch PaperBone marrow transplantationKupffer CellsLiver fibrosisdigestive systemCell LineBile Acids and Salts03 medical and health sciencesmedicineHepatic Stellate CellsAnimalsInflammationOrganic Chemistrymedicine.diseaseMolecular biologyTransplantationDisease Models Animal030104 developmental biologylcsh:Biology (General)Culture Media ConditionedNADPH oxidasesHepatic stellate cellbiology.proteinHepatocytesHepatic fibrosisReactive Oxygen Species030217 neurology & neurosurgeryBiomarkersRedox Biology
researchProduct

Modeling of Hepatocytes Proliferation Isolated from Proximal and Distal Zones from Human Hepatocellular Carcinoma Lesion

2016

Isolation of hepatocytes from cirrhotic human livers and subsequent primary culture are important new tools for laboratory research and cell-based therapeutics in the study of hepatocellular carcinoma (HCC). Using such techniques, we have previously identified different subpopulations of human hepatocytes and among them one is showing a progressive transformation of hepatocytes in HCC-like cells. We have hypothesized that increasing the distance from the neoplastic lesion might affect hepatocyte function and transformation capacity. However, limited information is available in comparing the growth and proliferation of human hepatocytes obtained from different areas of the same cirrhotic liv…

0301 basic medicineLiver CirrhosisMalePathologyCirrhosislcsh:MedicinePathology and Laboratory Medicine0302 clinical medicineAnimal CellsMedicine and Health SciencesTumor Cells Culturedlcsh:ScienceMultidisciplinaryLiver DiseasesFatty liverLiver NeoplasmsMiddle AgedLiverCirrhosisOncologyCell Processes030220 oncology & carcinogenesisHepatocellular carcinomaLiver FibrosisFemalemedicine.symptomCellular TypesAnatomyResearch Articlemedicine.medical_specialtyCarcinoma HepatocellularGastroenterology and HepatologyBiologyResearch and Analysis MethodsCarcinomasCell GrowthLesion03 medical and health sciencesSigns and SymptomsDiagnostic MedicineGastrointestinal TumorsmedicineCarcinomaHumansImmunohistochemistry TechniquesAgedCell ProliferationCell growthlcsh:RBiology and Life SciencesCancers and NeoplasmsCell BiologyHepatocellular Carcinomamedicine.diseaseProliferating cell nuclear antigenFatty LiverHistochemistry and Cytochemistry Techniques030104 developmental biologyCancer cellbiology.proteinHepatocytesImmunologic TechniquesLesionslcsh:QPLoS ONE
researchProduct

Loss of cellular FLICE-inhibitory protein promotes acute cholestatic liver injury and inflammation from bile duct ligation.

2017

Cholestatic liver injury results from impaired bile flow or metabolism and promotes hepatic inflammation and fibrogenesis. Toxic bile acids that accumulate in cholestasis induce apoptosis and contribute to early cholestatic liver injury, which is amplified by accompanying inflammation. The aim of the current study was to evaluate the role of the antiapoptotic caspase 8-homolog cellular FLICE-inhibitory (cFLIP) protein during acute cholestatic liver injury. Transgenic mice exhibiting hepatocyte-specific deletion of cFLIP (cFLIP−/−) were used for in vivo and in vitro analysis of cholestatic liver injury using bile duct ligation (BDL) and the addition of bile acids ex vivo. Loss of cFLIP in h…

0301 basic medicineLiver CirrhosisTime FactorsPhysiologyCASP8 and FADD-Like Apoptosis Regulating ProteinInflammationApoptosisp38 Mitogen-Activated Protein KinasesHepatitisBile Acids and Salts03 medical and health sciencesNecrosisCholestasisPhysiology (medical)medicineHepatic Stellate CellsAnimalsASK1Genetic Predisposition to DiseaseLigationCells CulturedTumor Necrosis Factor alpha-Induced Protein 3chemistry.chemical_classificationLiver injuryCommon Bile DuctMice KnockoutReactive oxygen speciesHepatologyBile duct ligationGastroenterologyTranscription Factor RelAmedicine.diseaseOxidative Stress030104 developmental biologyCholedocholithiasisPhenotypechemistryLiverNeutrophil InfiltrationApoptosisFLICE Inhibitory ProteinCancer researchHepatocytesCytokinesmedicine.symptomInflammation MediatorsSignal TransductionAmerican journal of physiology. Gastrointestinal and liver physiology
researchProduct

In Vivo siRNA Delivery to Immunosuppressive Liver Macrophages by alpha-Mannosyl-Functionalized Cationic Nanohydrogel Particles

2020

Macrophages are the front soldiers of the innate immune system and are vital for immune defense, tumor surveillance, and tissue homeostasis. In chronic diseases, including cancer and liver fibrosis, macrophages can be forced into an immunosuppressive and profibrotic M2 phenotype. M2-type macrophages overexpress the mannose receptor CD206. Targeting these cells via CD206 and macrophage repolarization towards an immune stimulating and antifibrotic M1 phenotype through RNA interference represents an appealing therapeutic approach. We designed nanohydrogel particles equipped with mannose residues on the surface (ManNP) that delivered siRNA more efficiently to M2 polarized macrophages compared t…

0301 basic medicineLiver CirrhosissiRNA deliveryTHP-1 Cellsmedicine.medical_treatmentmannose targetingMice0302 clinical medicineDrug Delivery SystemsFibrosisMacrophageM2 macrophagesRNA Small Interferinglcsh:QH301-705.5Tissue homeostasisMice Inbred BALB CChemistryHydrogelsGeneral MedicineHep G2 CellsLiver030220 oncology & carcinogenesisFemaleimmunotherapyMannose receptorMannose ReceptorReceptors Cell Surfacegene knock-downArticlenanohydrogels03 medical and health sciencesImmune systemIn vivomedicineImmune ToleranceAnimalsHumanscancerLectins C-TypeInnate immune systemMacrophagesfibrosisImmunotherapyMacrophage Activationmedicine.disease030104 developmental biologyMannose-Binding LectinsRAW 264.7 Cellslcsh:Biology (General)Cancer researchNanoparticlesMannose
researchProduct

Understanding the implication of autophagy in the activation of hepatic stellate cells in liver fibrosis: are we there yet?

2021

Liver fibrosis (LF) occurs as a result of persistent liver injury and can be defined as a pathologic, chronic, wound-healing process in which functional parenchyma is progressively replaced by fibrotic tissue. As a phenomenon involved in the majority of chronic liver diseases, and therefore prevalent, it exerts a significant impact on public health. This impact becomes even more patent given the lack of a specific pharmacological therapy, with LF only being ameliorated or prevented through the use of agents that alleviate the underlying causes. Hepatic stellate cells (HSCs) are fundamental mediators of LF, which, activated in response to pro-fibrotic stimuli, transdifferentiate from a quies…

0301 basic medicineLiver injuryLiver CirrhosisProgrammed cell deathCell cycle checkpointbusiness.industryAutophagymedicine.diseasePathology and Forensic Medicine03 medical and health sciences030104 developmental biology0302 clinical medicineCell culture030220 oncology & carcinogenesisLipid dropletCancer researchHepatic stellate cellmedicineAutophagyHepatic Stellate CellsAnimalsHumansbusinessMyofibroblastThe Journal of pathologyReferences
researchProduct

GRIP1 Binds to ApoER2 and EphrinB2 to Induce Activity-Dependent AMPA Receptor Insertion at the Synapse

2017

Summary Regulation of α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor trafficking in response to neuronal activity is critical for synaptic function and plasticity. Here, we show that neuronal activity induces the binding of ephrinB2 and ApoER2 receptors at the postsynapse to regulate de novo insertion of AMPA receptors. Mechanistically, the multi-PDZ adaptor glutamate-receptor-interacting protein 1 (GRIP1) binds ApoER2 and bridges a complex including ApoER2, ephrinB2, and AMPA receptors. Phosphorylation of ephrinB2 in a serine residue (Ser-9) is essential for the stability of such a complex. In vivo, a mutation on ephrinB2 Ser-9 in mice results in a complete disruption…

0301 basic medicineLong-Term PotentiationPrimary Cell CultureEphrin-B2Mice TransgenicNerve Tissue ProteinsephrinBAMPA receptorGRIP1BiologyHippocampusArticleApoER2General Biochemistry Genetics and Molecular BiologyPostsynapseMice03 medical and health sciences0302 clinical medicineddc:570SerineAnimalsReceptors AMPAPhosphorylationAMPA receptorsLong-term depressionlcsh:QH301-705.5LDL-Receptor Related ProteinsAdaptor Proteins Signal TransducingNeuronssynaptic plasticitySynaptic scalingLong-term potentiationCell biologyProtein Transport030104 developmental biologyGene Expression Regulationlcsh:Biology (General)nervous systemSynapsesSilent synapseSynaptic plasticityLTP030217 neurology & neurosurgeryIon channel linked receptorsProtein BindingSignal TransductionCell Reports
researchProduct