Search results for "disease model"

showing 10 items of 1116 documents

Cytomegalovirus vector expressing RAE-1γ induces enhanced anti-tumor capacity of murine CD8+ T cells

2017

Designing of CD8 T cell vaccines which would provide protection against tumors is still considered a great challenge in immunotherapy. Here we show a robust potential of a cytomegalovirus (CMV) vector expressing the NKG2D ligand RAE-1γ as CD8 T cell-based vaccine against malignant tumors. Immunization with the CMV vector expressing RAE-1γ delayed tumor growth or even provided complete protection against tumor challenge in both prophylactic and therapeutic settings. Moreover, a potent tumor control in mice vaccinated with this vector can be further enhanced by blocking the immune checkpoints TIGIT and PD-1. Expression of RAE-1γ by the CMV vector potentiated expansion of KLRG1+ CD8 T cells wi…

0301 basic medicineTumor vaccine [RAE-1γ]medicine.medical_treatmentT cellImmunologyGenetic VectorsProgrammed Cell Death 1 ReceptorMelanoma ExperimentalCytomegalovirusEpitopes T-LymphocyteBiologyCD8-Positive T-LymphocytesCancer VaccinesArticleCMV vectorNKG2DImmunomodulation03 medical and health sciencesMiceImmune systemTIGITKLRG1+ CD8+ T cellsNeoplasmsmedicineImmunology and AllergyCytotoxic T cellAnimalsHumansRAE-1γ : Tumor vaccineLectins C-TypeReceptors ImmunologicαTIGIT ; CMV vector ; KLRG1+ CD8+ T cells ; NKG2D ; RAE-1γ : Tumor vaccineBIOMEDICINE AND HEALTHCARE. Basic Medical Sciences.Membrane ProteinsImmunotherapyNKG2DVirology3. Good healthKiller Cells NaturalDisease Models Animal030104 developmental biologymedicine.anatomical_structureImmunizationAnimals NewbornFemaleαTIGITImmunotherapyBIOMEDICINA I ZDRAVSTVO. Temeljne medicinske znanosti.CD8
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Impact of the Usher syndrome on olfaction

2015

Usher syndrome is a genetically and clinically heterogeneous disease in humans, characterized by sensorineural hearing loss, retinitis pigmentosa and vestibular dysfunction. This disease is caused by mutations in genes encoding proteins that form complex networks in different cellular compartments. Currently, it remains unclear whether the Usher proteins also form networks within the olfactory epithelium (OE). Here, we describe Usher gene expression at the mRNA and protein level in the OE of mice and showed interactions between these proteins and olfactory signaling proteins. Additionally, we analyzed the odor sensitivity of different Usher syndrome mouse models using electro-olfactogram re…

0301 basic medicineUsher syndromeCell Cycle ProteinsMice TransgenicNerve Tissue ProteinsOlfactionMyosinsBiologyCell LineMice03 medical and health sciencesOlfactory MucosaGene expressionRetinitis pigmentosaotorhinolaryngologic diseasesGeneticsmedicineAnimalsHumansCiliaMolecular BiologyGeneGenetics (clinical)GeneticsExtracellular Matrix ProteinsMessenger RNAGene Expression ProfilingEpithelial CellsGeneral MedicineCadherinsmedicine.diseaseeye diseasesSmellCytoskeletal ProteinsDisease Models Animal030104 developmental biologymedicine.anatomical_structureGene Expression RegulationMyosin VIIaMutationOdorantsSignal transductionCarrier ProteinsUsher SyndromesOlfactory epitheliumSignal TransductionHuman Molecular Genetics
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Rescue of Hypovitaminosis A Induces Non-Amyloidogenic Amyloid Precursor Protein (APP) Processing.

2015

Retinoic acid, the bioactive metabolite of beta-carotene or vitamin A, plays a pleiotropic, multifunctional role in vertebrate development. Studies in rodents revealed that a diet deficient in vitamin A results in a complex neonatal syndrome (the VAD syndrome), manifested in many organs. In humans, the function of retinoic acid (RA) extends into adulthood, where it has important roles in fertility, vision, and suppression of neoplastic growth. In recent years, it has also been suggested that retinoic acid might potentially act as a therapeutically relevant drug in attenuating or even preventing neurodegenerative diseases such as Alzheimer's disease (AD). Here, we report that VAD leads to an…

0301 basic medicineVitaminmedicine.medical_specialtyADAM10Retinoic acidTretinoin03 medical and health scienceschemistry.chemical_compoundADAM10 ProteinAmyloid beta-Protein PrecursorMiceNeuroblastoma0302 clinical medicineKeratolytic AgentsTretinoinInternal medicineNeuroblastomaGene expressionPresenilin-2medicineAmyloid precursor proteinAnimalsHumansGene Regulatory NetworksRats WistarCells CulturedCerebral CortexNeuronsAmyloid beta-PeptidesbiologyVitamin A Deficiencymedicine.diseaseAcitretinPeptide FragmentsVitamin A deficiencyDisease Models Animal030104 developmental biologyEndocrinologyNeurologychemistryAnimals Newbornbiology.proteinFemaleNeurology (clinical)030217 neurology & neurosurgerymedicine.drugCurrent Alzheimer research
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C3 Drives Inflammatory Skin Carcinogenesis Independently of C5

2021

Nonmelanoma skin cancer such as cutaneous squamous cell carcinoma (cSCC) is the most common form of cancer and can occur as a consequence of DNA damage to the epithelium by UVR or chemical carcinogens. There is growing evidence that the complement system is involved in cancer immune surveillance; however, its role in cSCC remains unclear. Here, we show that complement genes are expressed in tissue from patients with cSCC, and C3 activation fragments are present in cSCC biopsies, indicating complement activation. Using a range of complement-deficient mice in a two-stage mouse model of chemically-induced cSCC, where a subclinical dose of 7,12-dimethylbenz[a]anthracene causes oncogenic mutatio…

0301 basic medicineWT wild typeSkin NeoplasmsComplement receptorComplement Membrane Attack Complexmedicine.disease_causeBiochemistrychemistry.chemical_compoundMice0302 clinical medicineCR complement receptorComplement ActivationSkinMice KnockoutcSCC cutaneous squamous cell carcinomaComplement C5Complement C3Receptors Complement030220 oncology & carcinogenesisCarcinoma Squamous CellDisease ProgressionTumor BiologyOriginal ArticleMAC membrane attack complexSignal TransductionHPV16 human papillomavirus type 16910-Dimethyl-12-benzanthraceneTPA 12-O-tetradecanoylphorbol-13-acetateMice TransgenicDermatologySettore MED/08 - Anatomia Patologica03 medical and health sciencesmedicineAnimalsHumansC3Molecular BiologyReceptor Anaphylatoxin C5aDMBA 712-dimethylbenz[a]anthracenebusiness.industry712-Dimethylbenz[a]anthraceneCancerCell BiologyNeoplasms Experimentalmedicine.diseaseComplement systemDisease Models Animal030104 developmental biologychemistryTumor progressionCancer researchCarcinogensTumor EscapeSkin cancerbusinessCarcinogenesisComplement membrane attack complexSkin carcinogenesis.EC epithelial cell
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Effects of muscular dystrophy, exercise and blocking activin receptor IIB ligands on the unfolded protein response and oxidative stress

2016

Protein homeostasis in cells, proteostasis, is maintained through several integrated processes and pathways and its dysregulation may mediate pathology in many diseases including Duchenne muscular dystrophy (DMD). Oxidative stress, heat shock proteins, endoplasmic reticulum (ER) stress and its response, i.e. unfolded protein response (UPR), play key roles in proteostasis but their involvement in the pathology of DMD are largely unknown. Moreover, exercise and activin receptor IIB blocking are two strategies that may be beneficial to DMD muscle, but studies to examine their effects on these proteostasis pathways are lacking. Therefore, these pathways were examined in the muscle of mdx mice, …

0301 basic medicineX-Box Binding Protein 1Activin Receptors Type IIEukaryotic Initiation Factor-2MyostatinUPRBiochemistryMiceeIF-2 KinaseThioredoxinsSirtuin 1ENDOPLASMIC-RETICULUM STRESSDISULFIDE-ISOMERASEPhosphorylationta315Endoplasmic Reticulum Chaperone BiPHeat-Shock ProteinsIN-VIVOta3141Activin receptorMOUSE MODELER STRESSEndoplasmic Reticulum Stress3. Good healthmedicine.anatomical_structuremyostatinPRESERVES MUSCLE FUNCTIONER-stressSKELETAL-MUSCLEmdxSignal TransductionEXPRESSIONmedicine.medical_specialtyXBP1MDX MICEBiologyProtein Serine-Threonine Kinases03 medical and health sciencesPhysiology (medical)Internal medicineHeat shock proteinPhysical Conditioning AnimalEndoribonucleasesmedicineAnimalsHumansRNA MessengerMuscle SkeletalSkeletal muscleMyostatinGENEActivating Transcription Factor 6Immunoglobulin Fc FragmentsMuscular Dystrophy DuchenneDisease Models Animal030104 developmental biologyProteostasisEndocrinologyGene Expression RegulationUnfolded protein responsebiology.proteinMice Inbred mdxProteostasisUnfolded Protein Response3111 BiomedicineCarrier ProteinsACVR2B
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7-ketocholesterol and 7β-hydroxycholesterol: in vitro and animal models used to characterize their activities and to identify molecules preventing th…

2020

International audience; Oxysterols are molecules derived by the oxidation of cholesterol and can be formed either by auto-oxidation, enzymatically or by both processes. Among the oxysterols formed by auto-oxidation, 7-ketocholesterol and 7beta-hydroxycholesterol are the main forms generated. These oxysterols, formed endogenously and brought in large quantities by certain foods, have major cytotoxic properties. They are powerful inducers of oxidative stress, inducing dysfunction of organelles (mitochondria, lysosomes and peroxisomes) that can cause cell death. These molecules are often identified in increased amounts in common pathological states such as cardiovascular diseases, certain eye …

0301 basic medicine[SDV]Life Sciences [q-bio]CellmicrofluidicMitochondrionPharmacologiemedicine.disease_causeBiochemistry0302 clinical medicineanimal modèleKetocholesterolsComputingMilieux_MISCELLANEOUSCells CulturedsignalingpathwaysCell DeathChemistry7β-hydroxycholesterolNeurodegenerative DiseasesPeroxisomeanimal models3. Good healthmedicine.anatomical_structureBiochemistryCardiovascular Diseases030220 oncology & carcinogenesisToxicity[SDV.NEU]Life Sciences [q-bio]/Neurons and Cognition [q-bio.NC]modèle cellulaireSignal transductionProgrammed cell deathCataractCell Line03 medical and health sciencesPharmaceutical sciencesCell Line TumormedicineAnimalsHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular Biologyhydroxycholestérol7-ketocholesterolPharmacologyOrganelles7-ketocholesterol;7β-hydroxycholesterol;cell models;animal models;microfluidic;signalingpathwaysInflammatory Bowel DiseasesIn vitroHydroxycholesterolscell modelsDisease Models Animal030104 developmental biologyvoie de signalisationSciences pharmaceutiques[SDV.AEN]Life Sciences [q-bio]/Food and NutritionOxidative stress
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Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice

2018

Fibrosis remains a serious health concern in patients with chronic liver disease. We recently reported that chemically induced chronic murine liver injury triggers increased expression of junctional adhesion molecules (JAMs) JAM-B and JAM-C by endothelial cells and de novo synthesis of JAM-C by hepatic stellate cells (HSCs). Here, we demonstrate that biopsies of patients suffering from primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) or autoimmune hepatitis (AIH) display elevated levels of JAM-C on portal fibroblasts (PFs), HSCs, endothelial cells and cholangiocytes, whereas smooth muscle cells expressed JAM-C constitutively. Therefore, localization and function of JA…

0301 basic medicine[SDV]Life Sciences [q-bio]Cholangitis SclerosingMyocytes Smooth MuscleeducationImmunologyImmunoglobulinsAutoimmune hepatitisVascular RemodelingChronic liver diseaseMural cellPrimary sclerosing cholangitisFatty Acids MonounsaturatedMice03 medical and health sciencesFibrosisCell AdhesionmedicineAnimalsHumansImmunology and AllergyMyofibroblastsCells CulturedInflammationMice KnockoutFibrous capsule of GlissonLiver Cirrhosis Biliarybusiness.industryfungiEndothelial Cellsmedicine.diseaseFibrosishumanities3. Good healthMice Inbred C57BLDisease Models AnimalHepatitis Autoimmune030104 developmental biologyLiverVasoconstrictioncardiovascular systemCancer researchHepatic stellate cellFemaleHepatic fibrosisbusinessCell Adhesion MoleculesJournal of Autoimmunity
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A new “sudden fright paradigm” to explore the role of (epi)genetic modulations of the DAT gene in fear-induced avoidance behavior

2020

Alterations in dopamine (DA) reuptake are involved in several psychiatric disorders whose symptoms can be investigated in knock out rats for the DA transporter (DAT-KO). Recent studies evidenced the role of epigenetic DAT modulation in depressive-like behavior. Accordingly, we used heterozygous (HET) rats born from both HET parents (termed MIX-HET), compared to HET rats born from WT-mother and KO-father (MAT-HET), implementing the role of maternal care on DAT modulation. We developed a "sudden fright" paradigm (based on dark-light test) to study reaction to fearful inputs in the DAT-KO, MAT-HET, MIX-HET, and WT groups. Rats could freely explore the whole 3-chambers apparatus; then, they wer…

0301 basic medicineanimal structuresEmotionsStimulus (physiology)Epigenesis GeneticReuptakechoice behavior03 medical and health sciencesBehavioral Neuroscience0302 clinical medicineDopamineDAT-KO ratAvoidance LearningGeneticsmedicineAnimalsFear conditioningEpigeneticsprefrontal cortex.Prefrontal cortexdopamine transporterDopamine transporterDopamine Plasma Membrane Transport ProteinsBehavior AnimalbiologyFearfear conditioningRatsDisease Models Animal030104 developmental biologyNeurologyAttention Deficit Disorder with Hyperactivitybiology.proteinSettore BIO/14 - Farmacologiaconditioned preferenceHistone deacetylaseNeuroscience030217 neurology & neurosurgerymedicine.drug
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Autophagy Stimulation as a Potential Strategy Against Intestinal Fibrosis

2019

We recently observed reduced autophagy in Crohn’s disease patients and an anti-inflammatory effect of autophagy stimulation in murine colitis, but both anti- and pro-fibrotic effects are associated with autophagy stimulation in different tissues, and fibrosis is a frequent complication of Crohn’s disease. Thus, we analyzed the effects of pharmacological modulation of autophagy in a murine model of intestinal fibrosis and detected that autophagy inhibition aggravates, while autophagy stimulation prevents, fibrosis. These effects are associated with changes in inflammation and in collagen degradation in primary fibroblasts. Thus, pharmacological stimulation of autophagy may be useful against …

0301 basic medicineautophagyStimulationInflammationDiseaseIntestinal fibrosis03 medical and health sciencesMice0302 clinical medicineCrohn DiseaseFibrosismedicineintestinal fibrosisMurine colitisAnimalslcsh:QH301-705.5Sirolimusbusiness.industryBrief ReportAutophagyGeneral MedicineFibroblastsmedicine.diseaseFibrosisIntestinesMice Inbred C57BLDisease Models Animal030104 developmental biologylcsh:Biology (General)inflammationCancer research030211 gastroenterology & hepatologyCollagenmedicine.symptomComplicationbusinessImmunosuppressive AgentsCells
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MECP2 impairs neuronal structure by regulating KIBRA

2016

Using a Drosophila model of MECP2 gain-of-function, we identified memory associated KIBRA as a target of MECP2 in regulating dendritic growth. We found that expression of human MECP2 increased kibra expression in Drosophila, and targeted RNAi knockdown of kibra in identified neurons fully rescued dendritic defects as induced by MECP2 gain-of-function. Validation in mouse confirmed that Kibra is similarly regulated by Mecp2 in a mammalian system. We found that Mecp2 gain-of-function in cultured mouse cortical neurons caused dendritic impairments and increased Kibra levels. Accordingly, Mecp2 loss-of-function in vivo led to decreased Kibra levels in hippocampus, cortex, and cerebellum. Togeth…

0301 basic medicinecongenital hereditary and neonatal diseases and abnormalitiesCerebellumMethyl-CpG-Binding Protein 2Dendritic morphologyHippocampusDisease modelsHippocampusArticlelcsh:RC321-571MECP2Mice03 medical and health sciencesMemoryRNA interferencemental disordersmedicineAnimalsHumanslcsh:Neurosciences. Biological psychiatry. NeuropsychiatryCerebral CortexNeuronsGene knockdownMECP2 duplication syndromebiologybiology.organism_classificationMECP2nervous system diseasesCortex (botany)Disease Models AnimalDrosophila melanogaster030104 developmental biologymedicine.anatomical_structureNeurologyCerebral cortexDrosophilaDrosophila melanogasterNeuroscienceNeurobiology of Disease
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