Search results for "Disease Model"

showing 10 items of 1116 documents

In vivo discovery of a peptide that prevents CUG-RNA hairpin formation and reverses RNA toxicity in myotonic dystrophy models

2011

6 pages, 5 figures. PMID:21730182[PubMed] PMCID: PMC3141925[Available on 2012/1/19]

congenital hereditary and neonatal diseases and abnormalitiesProtein ConformationRNA-binding proteinProtein Serine-Threonine KinasesBiologyMyotonic dystrophyMyotonin-Protein Kinasedrug discoveryMicechemistry.chemical_compoundnon-coding RNA diseasePeptide Librarymedicinal chemistryDrug DiscoveryGene expressionmedicineAnimalsMyotonic DystrophyMBNL1MultidisciplinaryMusclesdisease modelAlternative splicingRNA-Binding ProteinsRNADystrophyBiological Sciencesmedicine.diseaseRNA secondary structureMolecular biologyDNA-Binding ProteinschemistryRNA splicingDrosophilaTrinucleotide Repeat ExpansionOligopeptides
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Correction: Daunorubicin reduces MBNL1 sequestration caused by CUG-repeat expansion and rescues cardiac dysfunctions in a Drosophila model of myotoni…

2018

ABSTRACT Myotonic dystrophy (DM) is a dominantly inherited neuromuscular disorder caused by expression of mutant myotonin-protein kinase (DMPK) transcripts containing expanded CUG repeats. Pathogenic DMPK RNA sequesters the muscleblind-like (MBNL) proteins, causing alterations in metabolism of various RNAs. Cardiac dysfunction represents the second most common cause of death in DM type 1 (DM1) patients. However, the contribution of MBNL sequestration in DM1 cardiac dysfunction is unclear. We overexpressed Muscleblind (Mbl), the Drosophila MBNL orthologue, in cardiomyocytes of DM1 model flies and observed a rescue of heart dysfunctions, which are characteristic of these model flies and resem…

congenital hereditary and neonatal diseases and abnormalitiesRNA StabilityNeuroscience (miscellaneous)Medicine (miscellaneous)MuscleblindGeneral Biochemistry Genetics and Molecular BiologyImmunology and Microbiology (miscellaneous)AnimalsDrosophila ProteinsMyotonic DystrophyMyocytes CardiacRNA MessengerDaunorubicinCorrectionNuclear ProteinsReproducibility of ResultsHeartSurvival AnalysisAlternative SplicingDisease Models AnimalDrosophila melanogasterTrinucleotide repeat disorderDrosophilaTrinucleotide Repeat ExpansionResearch ArticleProtein BindingDisease Models & Mechanisms
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Human interleukin-6 facilitates hepatitis B virus infection in vitro and in vivo.

2000

Abstract Background and aim. Research on hepatitis B virus (HBV) infection in vivo has been limited due to the absence of a suitable animal model. We have developed a human–mouse radiation chimera in which normal mice, preconditioned by lethal total body irradiation and radioprotected with SCID mouse bone marrow cells, are permissive for engraftment of human hematopoietic cells and solid tissues. This resulting human–mouse model, which comprises three genetically disparate sources of tissue, is therefore termed Trimera. This study was aimed at assessing the effect of human IL-6 on HBV infection in vivo in Trimera mice. Methods. Trimera mice were transplanted with human liver tissue fragment…

endocrine systemHepatitis B virusMice SCIDmedicine.disease_causeVirus ReplicationMiceIn vivoVirologymedicineAnimalsHumansHepatitis B virusbiologychimeric miceInterleukin-6Hepatitis BVirologyMolecular biologydigestive system diseasesIn vitroTransplantationDisease Models Animalmedicine.anatomical_structureCell cultureRadiation Chimerabiology.proteinviral infectionBone marrowAntibodyviral receptorEx vivoVirology
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Review article: a comparison of glucagon-like peptides 1 and 2.

2013

Summary Background Recent advancements in understanding the roles and functions of glucagon-like peptide 1 (GLP-1) and 2 (GLP-2) have provided a basis for targeting these peptides in therapeutic strategies. Aim To summarise the preclinical and clinical research supporting the discovery of new therapeutic molecules targeting GLP-1 and GLP-2. Methods This review is based on a comprehensive PubMed search, representing literature published during the past 30 years related to GLP-1 and GLP-2. Results Although produced and secreted together primarily from L cells of the intestine in response to ingestion of nutrients, GLP-1 and GLP-2 exhibit distinctive biological functions that are governed by t…

endocrine systemmedia_common.quotation_subjectIncretinPharmacologyintestinal peptides GLP-1 GLP-2 incretin intestinal motilitySettore BIO/09 - FisiologiaIntestinal mucosaGlucagon-Like Peptide 1Glucagon-Like Peptide 2Receptors GlucagonAnimalsHumansMedicinePharmacology (medical)Molecular Targeted TherapyReceptormedia_commonClinical Trials as TopicHepatologybusiness.industrydigestive oral and skin physiologyGastroenterologyAppetiteReview articleDisease Models Animalmedicine.anatomical_structureGlucagon-Like PeptidesbusinessPancreashormones hormone substitutes and hormone antagonistsFunction (biology)
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Transgenic overexpression of corticotropin releasing hormone provides partial protection against neurodegeneration in an in vivo model of acute excit…

2008

Abstract Corticotropin releasing hormone (CRH) is the central modulator of the mammalian hypothalamic–pituitary–adrenal (HPA) axis. In addition, CRH affects other processes in the brain including learning, memory, and synaptic plasticity. Moreover, CRH has been shown to play a role in nerve cell survival under apoptotic conditions and to serve as an endogenous neuroprotectant in vitro . Employing mice overexpressing murine CRH in the CNS, we observed a differential response of CRH-overexpressing mice (CRH-COE hom -Nes) to acute excitotoxic stress induced by kainate compared with controls (CRH-COE con -Nes). Interestingly, CRH-overexpression reduced the duration of epileptic seizures and pre…

endocrine systemmedicine.medical_specialtyIndolesRNA UntranslatedCorticotropin-Releasing HormoneExcitotoxicityMice TransgenicNerve Tissue ProteinsBiologymedicine.disease_causeNeuroprotectionHippocampusNestinCorticotropin-releasing hormoneMiceIntermediate Filament ProteinsNeurotrophic factorsNeurofilament ProteinsSeizuresInternal medicineGlial Fibrillary Acidic Proteinpolycyclic compoundsmedicineExcitatory Amino Acid AgonistsReaction TimeAnimalsNeuroinflammationBrain-derived neurotrophic factorAnalysis of VarianceKainic AcidCell DeathGeneral NeuroscienceBrain-Derived Neurotrophic FactorNeurodegenerationProteinsLong-term potentiationmedicine.diseaseDisease Models AnimalEndocrinologynervous systemGene Expression RegulationNerve DegenerationNeurotoxicity SyndromesPlant Lectinshormones hormone substitutes and hormone antagonistsNeuroscience
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Inhibition of KIF20A by BKS0349 reduces endometriotic lesions in a xenograft mouse model

2019

AbstractSeveral studies have suggested a possible etiological association between ovarian endometriosis and ovarian cancer. Evidence has shown that KIF20A overexpression might confer a malignant phenotype to ovarian tumors by promoting proliferation and inhibiting apoptosis. However, no data about the role of KIF20A in endometriosis have been described. In this study, the human endometrium (n = 4) was transfected by mCherry adenovirus and intraperitoneally implanted in mice. Subsequently, mice were divided in three groups (n = 8/group) that were treated with Vehicle, BKS0349 (KIF20A-antagonist) or cabergoline (dopamine receptor agonist) for 21 days. mCherry-labeled endometriotic lesions wer…

endometriosisEmbryologyCabergolineEndometriosisEndometriosisKinesinsMice NudeApoptosisBiologyPeritoneal DiseasesEndometriumAndrologyEndometriumMiceGeneticsmedicineAnimalsHumansKIF20AMolecular BiologyCell ProliferationTUNEL assayOptical ImagingapoptosisObstetrics and GynecologyCell BiologyCell cyclemedicine.diseaseDisease Models Animalcell proliferationmedicine.anatomical_structureReproductive MedicineApoptosisOvarian EndometriosisHeterograftsImmunohistochemistrycell cycleFemaleOvarian cancerDevelopmental BiologyMolecular Human Reproduction
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Evaluation of PAI-1 in endometriosis using a homologous immunocompetent mouse model

2018

To analyze the role of PAI-1 (plasminogen activator inhibitor 1) in endometriotic lesion growth, we studied the effect of PAI-1 inhibition by PAI-039 using a homologous mouse model of endometriosis that allows noninvasive monitoring. Endometrial tissue from donor mice was collected, labeled with mCherry adenovirus, and implanted into a subcutaneous pocket on the ventral abdomen of recipient mice. Seven days after transplantation, mice were randomly allocated in two groups and treated once daily for 2 weeks with either vehicle (control group) or PAI-1 inhibitor (PAI-039 group). Endometriotic lesion size generated in recipient mice was monitored by mCherry signal. Animals were euthanized 21 d…

endometriosisPathologymedicine.medical_specialtyAngiogenesismouse modelnoninvasive monitoringEndometriosisEndometriosisPAI-1FibrinLesionNeovascularization03 medical and health scienceschemistry.chemical_compoundEndometriumMiceangiogenesis0302 clinical medicineIn vivoSerpin E2medicineAnimalsCell Proliferation030219 obstetrics & reproductive medicinebiologyIndoleacetic AcidsNeovascularization PathologicCell BiologyGeneral Medicinemedicine.diseaseTransplantationDisease Models AnimalReproductive Medicinechemistry030220 oncology & carcinogenesisPlasminogen activator inhibitor-1biology.proteinFemalefibrinolysismedicine.symptom
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The Inflammatory Feed-Forward Loop Triggered by the Complement Component C3 as a Potential Target in Endometriosis

2021

Copyright © 2021 Agostinis, Zorzet, Balduit, Zito, Mangogna, Macor, Romano, Toffoli, Belmonte, Morello, Martorana, Borelli, Ricci, Kishore and Bulla. The complement system is a major component of humoral innate immunity, acting as a first line of defense against microbes via opsonization and lysis of pathogens. However, novel roles of the complement system in inflammatory and immunological processes, including in cancer, are emerging. Endometriosis (EM), a benign disease characterized by ectopic endometrial implants, shows certain unique features of cancer, such as the capacity to invade surrounding tissues, and in severe cases, metastatic properties. A defective immune surveillance against…

endometriosisTHP-1 CellsTNF-amast cellsPeritoneal DiseasesCell DegranulationEndometriumImmunology and AllergyOriginal ResearchMice Knockoutmedicine.diagnostic_testendometriosiComplement C3Hep G2 CellsAntibody opsonizationmedicine.anatomical_structureComplement C3aTumor necrosis factor alphaFemaleInflammation MediatorsSignal TransductionImmunologyBiologySettore MED/08 - Anatomia PatologicaImmunofluorescencePeritoneal cavityPeritoneummedicineAnimalsHumansSettore MED/05 - Patologia ClinicaC3complement system...Innate immune systemTumor Necrosis Factor-alphaPeritoneal fluidC3; endometriosis; mast cells; complement system; TNF-aRC581-607Coculture TechniquesImmunity InnateComplement systemImmunity HumoralMice Inbred C57BLDisease Models AnimalCase-Control StudiesTNF-αCancer researchPeritoneal DiseaseImmunologic diseases. Allergymast cell
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Impact of

2018

Drosophila melanogaster has been for over a century the model of choice of several neurobiologists to decipher the formation and development of the nervous system as well as to mirror the pathophysiological conditions of many human neurodegenerative diseases. The rare disease Friedreich’s ataxia (FRDA) is not an exception. Since the isolation of the responsible gene more than two decades ago, the analysis of the fly orthologue has proven to be an excellent avenue to understand the development and progression of the disease, to unravel pivotal mechanisms underpinning the pathology and to identify genes and molecules that might well be either disease biomarkers or promising targets for therap…

frataxinDrug Evaluation PreclinicalFriedreich’s ataxiaReviewLipid Metabolismdrug screensDisease Models AnimalOxidative Stressendoplasmic reticulumDrosophila melanogasterPhenotypeironFriedreich AtaxiaIron-Binding Proteinsmetal homeostasisAnimalsHumansGenetic Predisposition to DiseaseGene Silencinggenetic screensInternational journal of molecular sciences
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Suppression and Replacement Gene Therapy for Autosomal Dominant Disease in a Murine Model of Dominant Retinitis Pigmentosa

2011

For dominantly inherited disorders development of gene therapies, targeting the primary genetic lesion has been impeded by mutational heterogeneity. An example is rhodopsin-linked autosomal dominant retinitis pigmentosa with over 150 mutations in the rhodopsin gene. Validation of a mutation-independent suppression and replacement gene therapy for this disorder has been undertaken. The therapy provides a means of correcting the genetic defect in a mutation-independent manner thereby circumventing the mutational diversity. Separate adeno-associated virus (AAV) vectors were used to deliver an RNA interference (RNAi)-based rhodopsin suppressor and a codon-modified rhodopsin replacement gene res…

genetic structuresGenetic enhancementMice TransgenicPolymerase Chain ReactionPhotoreceptor cellMiceRNA interferenceRetinitis pigmentosaDrug DiscoverymedicineGeneticsElectroretinographyAnimalsGeneMolecular BiologyPharmacologyGene therapy of the human retinabiologyAutosomal dominant traitGenetic Therapymedicine.diseaseMolecular biologyDisease Models Animalmedicine.anatomical_structureRhodopsinbiology.proteinMolecular MedicineOriginal Articlesense organsRetinitis PigmentosaMolecular Therapy
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