Search results for "Organoids"

showing 10 items of 32 documents

Interleukin 10 restores lipopolysaccharide-induced alterations in synaptic plasticity probed by repetitive magnetic stimulation

2020

Systemic inflammation is associated with alterations in complex brain functions such as learning and memory. However, diagnostic approaches to functionally assess and quantify inflammation-associated alterations in synaptic plasticity are not well-established. In previous work, we demonstrated that bacterial lipopolysaccharide (LPS)-induced systemic inflammation alters the ability of hippocampal neurons to express synaptic plasticity, i.e., the long-term potentiation (LTP) of excitatory neurotransmission. Here, we tested whether synaptic plasticity induced by repetitive magnetic stimulation (rMS), a non-invasive brain stimulation technique used in clinical practice, is affected by LPS-induc…

lcsh:Immunologic diseases. AllergyLipopolysaccharides0301 basic medicinenon-invasive brain stimulationInterleukin-1betaImmunologyTNFα-reporter mouseMice TransgenicStimulationNeurotransmissionHippocampusSynaptic TransmissionneuroinflammationInterferon-gammaMice03 medical and health sciences0302 clinical medicineGenes Reportertranscranial magnetic stimulationAnimalsImmunology and Allergyddc:610NeuroinflammationOriginal ResearchInflammationNeuronsNeuronal Plasticitysynaptic plasticityInterleukin-6Tumor Necrosis Factor-alphaChemistryLong-term potentiationInterleukin-10Mice Inbred C57BLOrganoids030104 developmental biologyBrain stimulationSynaptic plasticityExcitatory postsynaptic potentialTumor necrosis factor alphaMicrogliainterleukin 10lcsh:RC581-607Neuroscience030217 neurology & neurosurgery
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BCL-XL inhibition induces an FGFR4-mediated rescue response in colorectal cancer

2022

The heterogeneous therapy response observed in colorectal cancer is in part due to cancer stem cells (CSCs) that resist chemotherapeutic insults. The anti-apoptotic protein BCL-XL plays a critical role in protecting CSCs from cell death, where its inhibition with high doses of BH3 mimetics can induce apoptosis. Here, we screen a compound library for synergy with low-dose BCL-XL inhibitor A-1155463 to identify pathways that regulate sensitivity to BCL-XL inhibition and reveal that fibroblast growth factor receptor (FGFR)4 inhibition effectively sensitizes to A-1155463 both in vitro and in vivo. Mechanistically, we identify a rescue response that is activated upon BCL-XL inhibition and leads …

MaleBH3 mimeticsIndolesAxitinibColonDrug Evaluation Preclinicalbcl-X Proteincolorectal cancerMice SCIDGeneral Biochemistry Genetics and Molecular BiologyresistanceMice Inbred NODstem cellsCell Line TumorBCL-XLBCL-XL FGFR4 colorectal cancer apoptosis.AnimalsHumansReceptor Fibroblast Growth Factor Type 4BenzothiazolesAgedCell DeathDrug SynergismMiddle AgedIsoquinolinesOrganoidsNeoplastic Stem CellsFGFR4FemaleMCL-1Colorectal NeoplasmsCell reports
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ERK3/MAPK6 controls IL-8 production and chemotaxis

2020

ERK3 is a ubiquitously expressed member of the atypical mitogen activated protein kinases (MAPKs) and the physiological significance of its short half-life remains unclear. By employing gastrointestinal 3D organoids, we detect that ERK3 protein levels steadily decrease during epithelial differentiation. ERK3 is not required for 3D growth of human gastric epithelium. However, ERK3 is stabilized and activated in tumorigenic cells, but deteriorates over time in primary cells in response to lipopolysaccharide (LPS). ERK3 is necessary for production of several cellular factors including interleukin-8 (IL-8), in both, normal and tumorigenic cells. Particularly, ERK3 is critical for AP-1 signaling…

0301 basic medicineMAPK/ERK pathwayMouseQH301-705.5ScienceERK3General Biochemistry Genetics and Molecular BiologyCell Line03 medical and health sciencesMice0302 clinical medicineOrganoidmetastasisAnimalsHumansInterleukin 8Biology (General)chemotaxisMitogen-Activated Protein Kinase 6Gene knockdownGeneral Immunology and MicrobiologyIL-8ChemistryKinaseGeneral NeuroscienceQInterleukin-8RChemotaxisGeneral MedicineCell BiologyMAPKgastrointestinal organoidsIn vitroCell biologysecretomeChemotaxis Leukocyte030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisMedicineHeterograftsSignal transductionsignal transductionResearch ArticleHumaneLife
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Pattern of Invasion in Human Pancreatic Cancer Organoids Is Associated with Loss of SMAD4 and Clinical Outcome

2020

Abstract Pancreatic ductal adenocarcinoma (PDAC) is an aggressive malignancy characterized by extensive local invasion and systemic spread. In this study, we employed a three-dimensional organoid model of human pancreatic cancer to characterize the molecular alterations critical for invasion. Time-lapse microscopy was used to observe invasion in organoids from 25 surgically resected human PDAC samples in collagen I. Subsequent lentiviral modification and small-molecule inhibitors were used to investigate the molecular programs underlying invasion in PDAC organoids. When cultured in collagen I, PDAC organoids exhibited two distinct, morphologically defined invasive phenotypes, mesenchymal an…

0301 basic medicineCancer Researchendocrine system diseasesPancreatic ductal adenocarcinoma (PDAC)RAC1CDC42AdenocarcinomaBiologyArticle03 medical and health sciences0302 clinical medicineHuman Pancreatic CancerCell MovementPancreatic cancerBiomarkers TumorTumor Cells CulturedmedicineOrganoidHumansNeoplasm InvasivenessCell ProliferationSmad4 ProteinRegulation of gene expressionCell growthMesenchymal stem cellPrognosismedicine.diseasePhenotypedigestive system diseasesGene Expression Regulation NeoplasticOrganoidsPancreatic NeoplasmsSurvival Rate030104 developmental biologyOncology030220 oncology & carcinogenesisembryonic structuresCancer researchCarcinoma Pancreatic DuctalSignal TransductionCancer Research
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Breast Cancer Organoids Model Patient-Specific Response to Drug Treatment

2020

Tumor organoids are tridimensional cell culture systems that are generated in vitro from surgically resected patients&rsquo

0301 basic medicineCancer ResearchMechanotransductionBreast cancer; Dasatinib; Drug testing; Heterogeneity; Mechanotransduction; Patient‐derived tumor organoids; Statin; YAPPatient‐derived tumor organoidCellDasatinibDrug resistanceSettore MED/08 - Anatomia PatologicaBiologylcsh:RC254-282Article03 medical and health sciencesBreast cancer0302 clinical medicineBreast cancerbreast cancermedicineOrganoidSettore MED/05 - Patologia Clinicadasatinibdrug testingmechanotransductionpatient-derived tumor organoidsGenetic heterogeneitystatinStatinDrug testingBreast cancerDasatinib Drug testing Drug testing Heterogeneity Patient‐derived tumor organoids Statin YAPmedicine.diseaselcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensIn vitroDasatinib030104 developmental biologymedicine.anatomical_structureOncologyCell culture030220 oncology & carcinogenesisCancer researchPatient‐derived tumor organoidsYAPHeterogeneityheterogeneitymedicine.drugCancers
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Lack of "Synaptic" Ribbons in the Pineal Gland of BALB/c Mice

1988

In mammalian pinealocytes "synaptic" ribbons (SR) are regularly occurring organelles that are functionally poorly understood. Since in a number of studies on the mouse pineal gland the presence of SR has not been mentioned, it was the aim of this investigation to quantitate SR in mice. BALB/c mice were chosen, which have recently been shown to have a genetic defect for melatonin synthesis. The pineals of 15 mice killed at night, when SR numbers are normally high, were examined electron microscopically, scanning an area of greater than 20,000 micron 2 per gland. In none of these pineals were SR detected. It is concluded that the lack or extreme rarity of SR in laboratory mice may be related …

endocrine systemmedicine.medical_specialtyRatónCell CommunicationPineal GlandBALB/cPinealocyteMelatoninSynapseMicePineal glandEndocrinologyInternal medicineOrganoidmedicineAnimalsMelatoninMice Inbred BALB Cbiologybiology.organism_classificationOrganoidsEndocrinologymedicine.anatomical_structureUltrastructureFemalehormones hormone substitutes and hormone antagonistsmedicine.drugJournal of Pineal Research
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Signalling codes for the maintenance and lineage commitment of embryonic gastric epithelial progenitors

2020

The identity of embryonic gastric epithelial progenitors is unknown. We used single-cell RNA sequencing, genetic lineage tracing and organoid assays to assess whether Axin2 and Lgr5 expressing cells are gastric progenitors in the developing mouse stomach. We show that Axin2+ cells represent a transient population of embryonic epithelial cells in the forestomach. Lgr5+ cells generate both glandular corpus and squamous forestomach organoids ex vivo. Only Lgr5+ progenitors give rise to zymogenic cells in culture. Modulating the activity of the WNT, BMP and Notch pathways in vivo and ex vivo, we found that WNTs are essential for the maintenance of Lgr5+ epithelial cells. Notch prevents differen…

Lineage (genetic)PopulationCell fate determinationBiologyMice03 medical and health sciences0302 clinical medicineAnimalsCell LineageProgenitor celleducationMolecular Biology030304 developmental biology0303 health scienceseducation.field_of_studyStem CellsStomachLGR5Wnt signaling pathwayCell DifferentiationEpithelial CellsEmbryonic stem cellCell biologyOrganoidsGastric Mucosa030220 oncology & carcinogenesisFemaleEx vivoSignal TransductionDevelopmental BiologyDevelopment
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Pharmacological targeting of the novel β-catenin chromatin-associated kinase p38α in colorectal cancer stem cell tumorspheres and organoids

2021

AbstractThe prognosis of locally advanced colorectal cancer (CRC) is currently unsatisfactory. This is mainly due to drug resistance, recurrence, and subsequent metastatic dissemination, which are sustained by the cancer stem cell (CSC) population. The main driver of the CSC gene expression program is Wnt signaling, and previous reports indicate that Wnt3a can activate p38 MAPK. Besides, p38 was shown to feed into the canonical Wnt/β-catenin pathway. Here we show that patient-derived locally advanced CRC stem cells (CRC-SCs) are characterized by increased expression of p38α and are “addicted” to its kinase activity. Of note, we found that stage III CRC patients with high p38α levels display…

Cancer ResearchSettore MED/06 - Oncologia Medicapost-translationalImmunologyPopulationSynthetic lethalityArticleCellular and Molecular NeuroscienceCancer stem cellchromatin; colorectal neoplasms; humans; mitogen-activated protein kinase 14; neoplastic stem cells; organoids; prognosis; protein processing post-translational; beta cateninMedicineKinase activitycolon cancer p38 cancer stem cellslcsh:QH573-671educationhumansmitogen-activated protein kinase 14organoidsTrametinibSettore MED/04 - Patologia Generaleeducation.field_of_studybusiness.industrylcsh:CytologyCancer stem cellsneoplastic stem cellsWnt signaling pathwayprotein processingCell Biologycolorectal neoplasmsColorectal cancerdigestive system diseasesSettore BIO/12 - Biochimica Clinica E Biologia Molecolare ClinicaCateninCancer researchbeta cateninchromatinprognosisStem cellSettore MED/46 - Scienze Tecniche Di Medicina Di LaboratoriobusinessProtein Processing Post-TranslationalPost-translational modifications
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Filipin labelling and intramembrane particles on the membranes of early and later autophagic vacuoles in Ehrlich ascites cells

1987

Cholesterol and intramembrane particle distribution on autophagic vacuole membranes was studied in Ehrlich ascites cells using filipin labelling and freeze-fracture electron microscopy. Unsaturated fatty acids were stained using imidazole-buffered osmium tetroxide. Autophagocytosis was induced with vinblastine, and early autophagic vacuoles were accumulated by lowering the ATP level in the cells with iodoacetate. Filipin labelling was observed in the limiting membranes of later, apparently hydrolase-containing autophagic vacuoles, whereas the most newly-formed, doublemembrane limited vacuoles were not labelled. The limiting membranes of late, residual body-type vacuoles either showed patchy…

Osmium TetroxideIodoacetatesPolyenesVacuoleBiologyVinblastineFilipinlaw.inventionMembrane LipidsMice03 medical and health scienceschemistry.chemical_compoundPhagocytosislawAutophagyAnimalsFreeze FracturingFilipinCarcinoma Ehrlich Tumor030304 developmental biology0303 health sciencesStaining and LabelingCholesterolEndoplasmic reticulum030302 biochemistry & molecular biologyAutophagyImidazolesMembrane ProteinsIntracellular MembranesCell biologyOrganoidsMicroscopy ElectronCholesterolMembranechemistryOsmium tetroxideVacuolesElectron microscopeVirchows Archiv B Cell Pathology Including Molecular Pathology
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Cerebriform sebaceous nevus: a subtype of organoid nevus due to specific postzygotic FGFR2 mutations.

2021

Background Postzygotic mutations in FGFR2 have been identified in mosaic forms of acne, keratinocytic epidermal nevi, nevoid acanthosis nigricans / rounded and velvety epidermal nevus and in two fetuses with papillomatous pedunculated sebaceous nevus (PPSN). Objectives To determine the clinical and genetic characteristics of children with cerebriform, papillomatous, and pedunculated variants of sebaceous nevi. Methods Infants diagnosed with sebaceous nevi characterized by a cerebriform, papillomatous, and/or pedunculated morphology over a 10-year period (2010 - 2019) at three pediatric dermatology centers in Switzerland and France were included in this case series. Clinical and histological…

medicine.medical_specialtySkin NeoplasmsCutis gyrataDermatologyEpidermal nevusmedicine.disease_causeGermline030207 dermatology & venereal diseases03 medical and health sciences0302 clinical medicinemedicineNevusHumansPediatric dermatologyReceptor Fibroblast Growth Factor Type 2skin and connective tissue diseasesAcanthosis nigricansNevusMutationintegumentary systembusiness.industryOrganoid Nevusmedicine.diseaseDermatologyOrganoidsInfectious Diseases030220 oncology & carcinogenesisMutationbusinessJournal of the European Academy of Dermatology and Venereology : JEADVReferences
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