Search results for "Type I"

showing 10 items of 966 documents

New insights into the mechanism of action of pyrazolo[1,2-a]benzo[1,2,3,4]tetrazin-3-one derivatives endowed with anticancer potential

2018

Due to the scarce biological profile, the pyrazolo[1,2-a]benzo[1,2,3,4]tetrazine-3-one scaffold (PBT) has been recently explored as promising core for potential anticancer candidates. Several suitably decorated derivatives (PBTs) exhibited antiproliferative activity in the low-micromolar range associated with apoptosis induction and cell cycle arrest on S phase. Herein, we selected the most active derivatives and submitted them to further biological explorations to deepen the mechanism of action. At first, a DNA targeting is approached by means of flow Linear Dichroism experiments so as to evaluate how small planar molecules might interact with DNA, including the interference with the catal…

0301 basic medicineCell cycle checkpointPyrazolo[1TetrazolesBiochemistrychemistry.chemical_compound0302 clinical medicineSalmonAntiproliferative; DNA-interacting; Intercalation; Linear dichroism; Molecular docking; Pyrazolo[12-a]benzo[1234]tetrazin-3-one; Topoisomerase II; Biochemistry; Molecular MedicineDrug DiscoveryDNA-interactingBase PairingADMEbiologyIntercalating AgentsMolecular Docking Simulation030220 oncology & carcinogenesisMolecular Medicinemedicine.symptomtopoisomerase II3StereochemistryIn silico2Antineoplastic Agentslinear dichroism03 medical and health sciencesantiproliferativeintercalationmedicineAnimalsHumansDNA Cleavage2-a]benzo[1Pharmacology4]tetrazin-3-oneBinding SitesTopoisomeraseOrganic ChemistryDNAmolecular dockingSettore CHIM/08 - Chimica FarmaceuticaChemical spaceProtein Structure TertiaryDNA Topoisomerases Type II030104 developmental biologyMechanism of actionchemistryCatalytic cyclebiology.proteinpyrazolo[12-a]benzo[1234]tetrazin-3-oneDNAChemical Biology & Drug Design
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Visualizing In Vitro Type I Collagen Fibrillogenesis by Transmission Electron Microscopy

2017

Techniques and protocols for the in vitro formation of collagen type I fibrils and the extensive biochemical variation of the fibrillogenesis conditions are presented. In all cases, the incubation and fibrillogenesis product can be readily monitored by transmission electron microscopic study of negatively stained specimens. Representative TEM data is presented and discussed within the context of the products of the fibrillogenesis protocols, from which the extensive biochemical and structural possibilities of this integrated approach can be appreciated.

0301 basic medicineChemistryfood and beveragesFibrillogenesisContext (language use)02 engineering and technology021001 nanoscience & nanotechnologyFibrilNegative stainIn vitrolaw.invention03 medical and health sciences030104 developmental biologyTransmission electron microscopylawBiophysicsElectron microscope0210 nano-technologyType I collagen
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Modification of DNA structure by reactive nitrogen species as a result of 2-methoxyestradiol–induced neuronal nitric oxide synthase uncoupling in met…

2020

Abstract 2-methoxyestradiol (2-ME) is a physiological anticancer compound, metabolite of 17β-estradiol. Previously, our group evidenced that from mechanistic point of view one of anticancer mechanisms of action of 2-ME is specific induction and nuclear hijacking of neuronal nitric oxide synthase (nNOS), resulting in local generation of nitro-oxidative stress and finally, cancer cell death. The current study aims to establish the substantial mechanism of generation of reactive nitrogen species by 2-ME. We further achieved to identify the specific reactive nitrogen species involved in DNA-damaging mechanism of 2-ME. The study was performed using metastatic osteosarcoma 143B cells. We detected…

0301 basic medicineDNA damageClinical BiochemistryBone NeoplasmsNitric Oxide Synthase Type INitric OxideBiochemistryNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicinePeroxynitrous AcidHumansMTT assayViability assaylcsh:QH301-705.5Reactive nitrogen speciesSettore CHIM/02 - Chimica FisicaOsteosarcomalcsh:R5-920Settore BIO/16 - Anatomia UmanaOrganic ChemistryDNAReactive Nitrogen Species2-MethoxyestradiolPeroxynitrous acid030104 developmental biologychemistrylcsh:Biology (General)Settore CHIM/03 - Chimica Generale E InorganicaCancer cellBiophysicslcsh:Medicine (General)030217 neurology & neurosurgeryPeroxynitrite2 methoxyestradiol nitric oxide chemotherapyResearch PaperRedox Biology
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Microparticles harbouring Sonic hedgehog morphogen improve the vasculogenesis capacity of endothelial progenitor cells derived from myocardial infarc…

2019

Aims Endothelial progenitor cells (EPC) play a role in endothelium integrity maintenance and regeneration. Decreased numbers of EPC or their impaired function correlates with an increase in cardiovascular events. Thus, EPC are important predictors of cardiovascular mortality and morbidity. Microparticles carrying Sonic hedgehog (Shh) morphogen (MPShh+) trigger pro-angiogenic responses, both in endothelial cells and in ischaemic rodent models. Here, we propose that MPShh+ regulates EPC function, thus enhancing vasculogenesis, and correcting the defects in dysfunctional EPC obtained from acute myocardial infarction (AMI) patients. Methods and results The mechanisms underlying Shh pathway func…

0301 basic medicineEndotheliumNitric Oxide Synthase Type IIIPhysiologyAngiogenesis[SDV]Life Sciences [q-bio]Myocardial InfarctionMice NudeNeovascularization PhysiologicAcute myocardial infarction030204 cardiovascular system & hematologyMicroparticlesZinc Finger Protein GLI103 medical and health sciences0302 clinical medicineVasculogenesisCell-Derived MicroparticlesPhysiology (medical)Paracrine CommunicationVasculogenesismedicineAnimalsHumansHedgehog ProteinsProgenitor cellSonic hedgehogAngiogenic ProteinsCells CulturedComputingMilieux_MISCELLANEOUSEndothelial progenitor cellsbiologybusiness.industryNitric oxideSmoothened ReceptorHedgehog signaling pathwayPatched-1 ReceptorVascular endothelial growth factor A030104 developmental biologymedicine.anatomical_structureCase-Control StudiesKLF2embryonic structuresCancer researchbiology.proteincardiovascular systemCardiology and Cardiovascular MedicinebusinessSignal Transductioncirculatory and respiratory physiology
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Small molecule inhibitors and stimulators of inducible nitric oxide synthase in cancer cells from natural origin (phytochemicals, marine compounds, a…

2019

Nitric oxide synthases (NOS) are a family of isoforms, which generate nitric oxide (NO). NO is one of the smallest molecules in nature and acts mainly as a potent vasodilator. It participates in various biological processes ranging from physiological to pathological conditions. Inducible NOS (iNOS, NOS2) is a calcium-independent and inducible isoform. Despite high iNOS expression in many tumors, the role of iNOS is still unclear and complex with both enhancing and prohibiting actions in tumorigenesis. Nature presents a broad variety of natural stimulators and inhibitors, which may either promote or inhibit iNOS response. In the present review, we give an overview of iNOS-modulating agents w…

0301 basic medicineGene isoformPhytochemicalsNitric Oxide Synthase Type IIVasodilationmedicine.disease_causeBiochemistryNitric oxide03 medical and health scienceschemistry.chemical_compound0302 clinical medicineNeoplasmsmedicineAnimalsHumansEnzyme InhibitorsPharmacologyBiological ProductsNatural productMolecular StructurebiologySmall moleculeAnti-Bacterial AgentsEnzyme ActivationNitric oxide synthase030104 developmental biologyBiochemistrychemistry030220 oncology & carcinogenesisCancer cellbiology.proteinCarcinogenesisBiochemical Pharmacology
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Inducible knockdown of procollagen I protects mice from liver fibrosis and leads to dysregulated matrix genes and attenuated inflammation.

2017

Organ fibrosis is characterized by a chronic wound-healing response, with excess deposition of extracellular matrix components. Here, collagen type I represents the most abundant scar component and a primary target for antifibrotic therapies. Liver fibrosis can progress to cirrhosis and primary liver cancer, which are the major causes of liver related morbidity and mortality. However, a (pro-)collagen type I specific therapy remains difficult and its therapeutic abrogation may incur unwanted side effects. We therefore designed tetracycline-regulated procollagen alpha1(I) short hairpin (sh)RNA expressing mice that permit a highly efficient inducible knockdown of the procollagen alpha1(I) gen…

0301 basic medicineGenetically modified mouseLiver CirrhosisPathologymedicine.medical_specialtyCirrhosisInflammationMice TransgenicCollagen Type ISmall hairpin RNAExtracellular matrix03 medical and health sciencesMiceFibrosismedicineAnimalsRNA Small InterferingMolecular BiologyCells CulturedGene knockdownExtracellular Matrix ProteinsChemistryMouse Embryonic Stem CellsFibroblastsmedicine.diseaseProcollagen peptidaseDisease Models Animal030104 developmental biologyGene Expression RegulationGene Knockdown TechniquesCancer researchmedicine.symptomProcollagenMatrix biology : journal of the International Society for Matrix Biology
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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Measles in Italy: Viral strains and crossing borders

2019

In 2017, Italy experienced one of the largest outbreaks of measles in recent years, with 5404 notified cases and 4347 confirmed cases. A further 2029 cases were notified during the first 6 months of 2018, and 1516 of them were laboratory-confirmed. The B3 and D8 genotypes were identified as those responsible for the outbreak. Possible transmission routes can be established by monitoring the circulating measles virus strains in support of the national health authorities to warn people and travellers. Keywords: Outbreak, Measles, Genotype identification, Surveillance

0301 basic medicineGenotyping TechniquesWHO/EuropeSettore MED/42 - Igiene Generale E ApplicataDisease OutbreaksWHO0302 clinical medicineMeasleGenotype030212 general & internal medicineTravelSurveillancebiologyTransmission (medicine)General MedicineEmigration and ImmigrationInfectious DiseasesGenotype identificationItalyWorld Health Organization European RegionSequence AnalysisMicrobiology (medical)medicine.medical_specialtyGenotype030106 microbiologyWorld Health OrganizationMeasleslcsh:Infectious and parasitic diseasesEuropean Regional Verification Commission for Measles and Rubella Elimination; Genotype identification; MeaNS; Measles; Measles Nucleotide Surveillance; Outbreak; RVC; Surveillance; WHO; WHO/Europe; World Health Organization; World Health Organization European RegionOutbreak Measles Genotype identification SurveillanceMeasles virus03 medical and health sciencesGenotype identification; Measles; Outbreak; Surveillance; Emigration and Immigration; Genotype; Genotyping Techniques; Humans; Italy; Measles; Measles virus; Sequence Analysis DNA; Travel; Disease OutbreaksmedicineHumanslcsh:RC109-216Genotyping TechniquesMeaNSNational healthEuropean Regional Verification Commission for Measles and Rubella EliminationPublic healthOutbreakOutbreakSequence Analysis DNADNAmedicine.diseasebiology.organism_classificationVirologyRVCMeasles virusMeasles Nucleotide SurveillanceMeasles
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Structures of collagen IV globular domains: insight into associated pathologies, folding and network assembly

2018

15 páginas, 6 figuras, 1 tabla.

0301 basic medicineGoodpasture’s diseaseAddenda and ErrataRandom hexamerBiochemistryEpitopelaw.invention03 medical and health sciencesAlport's syndrome0302 clinical medicineGoodpasture's diseaselawMissense mutationGeneral Materials ScienceAlport’s syndromeStructural motifNetwork assemblyCrystallographyGoodpasture's diseaseChemistry(IV)NC1 hexamersStructural proteinCollagen type IVGeneral ChemistryCondensed Matter PhysicsResearch PapersFolding (chemistry)030104 developmental biologyQD901-999BiophysicsRecombinant DNA030217 neurology & neurosurgeryAlport syndrome
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Donor interleukin-22 and host type I interferon signaling pathway participate in intestinal graft-versus-host disease via STAT1 activation and CXCL10.

2014

Acute graft-versus-host disease (aGVHD) remains a major complication following allogeneic hematopoietic cell transplantation, limiting the success of this therapy. We previously reported that interleukin-22 (IL-22) participates to aGVHD development, but the underlying mechanisms of its contribution remain poorly understood. In this study, we analyzed the mechanism of the pathological function of IL-22 in intestinal aGVHD. Ex-vivo colon culture experiments indicated that IL-22 was able to induce Th1-like inflammation via signal transducer and activator of transcription factor-1 (STAT1) and CXCL10 induction in the presence of type I interferon (IFN). To evaluate a potential synergy between IL…

0301 basic medicineImmunologyGraft vs Host DiseaseInflammationReceptor Interferon alpha-betaInterleukin 2203 medical and health sciencesMiceInterferonimmune system diseasesBone MarrowmedicineImmunology and AllergyCXCL10AnimalsTransplantation HomologousHumansSTAT1Intestine LargeIntestinal MucosaBone Marrow TransplantationMice KnockoutMice Inbred BALB CbiologyInterleukinsTh1 CellsTissue DonorsTransplantationMice Inbred C57BLChemokine CXCL10030104 developmental biologymedicine.anatomical_structuresurgical procedures operativeSTAT1 Transcription FactorGene Expression RegulationHematologic NeoplasmsImmunologyInterferon Type Ibiology.proteinSTAT proteinBone marrowmedicine.symptomWhole-Body Irradiationmedicine.drugSignal Transduction
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