Search results for "CHON"

showing 10 items of 1866 documents

Phosphoproteomics of the developing heart identifies PERM1 - An outer mitochondrial membrane protein.

2021

Heart development relies on PTMs that control cardiomyocyte proliferation, differentiation and cardiac morphogenesis. We generated a map of phosphorylation sites during the early stages of cardiac postnatal development in mice; we quantified over 10,000 phosphorylation sites and 5000 proteins that were assigned to different pathways. Analysis of mitochondrial proteins led to the identification of PGC-1- and ERR-induced regulator in muscle 1 (PERM1), which is specifically expressed in skeletal muscle and heart tissue and associates with the outer mitochondrial membrane. We demonstrate PERM1 is subject to rapid changes mediated by the UPS through phosphorylation of its PEST motif by casein ki…

0301 basic medicineProteomicsOrganogenesisMFN2Muscle ProteinsP70-S6 Kinase 1030204 cardiovascular system & hematologyMitochondrionMitochondria Heart03 medical and health sciencesMice0302 clinical medicineCa2+/calmodulin-dependent protein kinaseAnimalsMolecular BiologyMitochondrial transportMice KnockoutChemistryMyocardiumPhosphoproteomicsMembrane ProteinsHeartLipid MetabolismPhosphoproteinsSolute carrier familyCell biology030104 developmental biologyMitochondrial MembranesPhosphorylationCardiology and Cardiovascular MedicineJournal of molecular and cellular cardiology
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Metabolic and inflammatory reprogramming of macrophages by ONC201 translates in a pro-inflammatory environment even in presence of glioblastoma cells

2020

Tumor-associated macrophages facilitate tumor progression and resistance to therapy. Their capacity for metabolic and inflammatory reprogramming represents an attractive therapeutic target. ONC201/TIC10 is an anticancer molecule that antagonizes the dopamine receptor D2 and affects mitochondria integrity in tumor cells. We examined whether ONC201 induces a metabolic and pro-inflammatory switch in primary human monocyte-derived macrophages that reactivates their antitumor activities, thus enhancing the onco-toxicity of ONC201. Contrary to glioblastoma cells, macrophages exhibited a low ratio of dopamine receptors D2/D5 gene expression and were resistant to ONC201 cytotoxicity. Macrophages re…

0301 basic medicinePyridinesImmunology610 MedizinGlutamic AcidAntineoplastic AgentsMitochondrionBiology570 Life sciences03 medical and health sciences0302 clinical medicineImmune systemCell Line TumorDopamine receptor D2610 Medical sciencesTumor MicroenvironmentHumansImmunology and AllergyMacrophageReceptors Dopamine D5Tumor microenvironmentReceptors Dopamine D2MacrophagesImidazolesMitochondriaCell biologyGene Expression Regulation NeoplasticPyrimidines030104 developmental biologyDrug Resistance NeoplasmTumor progressionDopamine receptorEnergy MetabolismGlioblastomaReprogrammingTranscription Factor CHOPSignal Transduction030215 immunology570 Biowissenschaften
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Cytotoxic activity of the histone deacetylase 3-Selective inhibitor Pojamide on MDA-MB-231 triple-negative breast cancer cells

2019

We examined the effects of the ferrocene-based histone deacetylase-3 inhibitor Pojamide (N1-(2-aminophenyl)-N8-ferrocenyloctanediamide) and its two derivatives N1-(2-aminophenyl)-N6-ferrocenyladipamide and N1-(2-aminophenyl)-N8-ferroceniumoctanediamide tetrafluoroborate on triple-negative MDA-MB-231 breast cancer cells. Viability/growth assays indicated that only the first two compounds at 70 &mu

0301 basic medicineQD0901Triple Negative Breast Neoplasmslcsh:Chemistry0302 clinical medicinebreast cancer cellmitochondrial transmembrane potentialCytotoxic T cellQDSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopyTriple-negative breast cancerreactive oxygen speciesCell DeathChemistryHistone deacetylase inhibitorQapoptosisGeneral MedicineCell cycle3. Good healthComputer Science Applications030220 oncology & carcinogenesisFemalecell cycleProgrammed cell deathautophagymedicine.drug_classCell SurvivalCatalysisArticleHistone DeacetylasesInorganic Chemistry03 medical and health sciencesCell Line TumormedicineBiomarkers TumorHumansViability assayPhysical and Theoretical ChemistryMolecular Biologyhistone deacetylase inhibitorcell viabilityOrganic ChemistryAutophagyapoptosiMatrix MetalloproteinasesHistone Deacetylase InhibitorsSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999ApoptosisCancer researchQD0146breast cancer cells
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Recovery from Toxic-Induced Demyelination Does Not Require the NG2 Proteoglycan

2016

NG2 cells are defined as CNS cells expressing chondroitin sulfate proteoglycan nerve/glia antigen. The vast majority of NG2-positive cells also express platelet-derived growth factor receptor alpha (PDGFRα) and are oligodendroglial progenitors (OPC). In addition a subpopulation of pericytes expresses NG2, but is positive for PDGF receptor beta (PDGFRβ) [1]. NG2-positive OPC comprise approximately 5% of the cells in the CNS where they are evenly distributed in grey and white matter [2, 3]. NG2-positive OPC form synapses with neurons [4–6] and react to brain injury with proliferation, as has been shown in several animal models as well as in human demyelinating and degenerative diseases [7–9].…

0301 basic medicineReceptor Platelet-Derived Growth Factor alphaCellular differentiationlcsh:MedicineGene ExpressionMice TransgenicOLIG203 medical and health scienceschemistry.chemical_compoundCuprizone0302 clinical medicineCell MovementExtracellularmedicineAnimalsRemyelinationAntigenslcsh:ScienceCells CulturedCell ProliferationMice KnockoutMultidisciplinarybiologyMicrogliaReverse Transcriptase Polymerase Chain ReactionStem Cellslcsh:RBrainCorrectionCell DifferentiationImmunohistochemistryCell biologyMicroscopy ElectronOligodendroglia030104 developmental biologymedicine.anatomical_structurenervous systemchemistryChondroitin sulfate proteoglycanCell cultureImmunologybiology.proteinlcsh:QProteoglycans030217 neurology & neurosurgeryPlatelet-derived growth factor receptorDemyelinating DiseasesPloS one
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Biological performance of cell-encapsulated methacrylated gellan gum-based hydrogels for nucleus pulposus regeneration

2014

Limitations of current treatments for intervertebral disc (IVD) degeneration have promoted interest in the development of tissue-engineering approaches. Injectable hydrogels loaded with cells can be used as a substitute material for the inner IVD part, the nucleus pulposus (NP), and provide an opportunity for minimally invasive treatment of IVD degeneration. The NP is populated by chondrocyte-like cells; therefore, chondrocytes and mesenchymal stem cells (MSCs), stimulated to differentiate along the chondrogenic lineage, could be used to promote NP regeneration. In this study, the in vitro and in vivo response of human bone marrow-derived MSCs and nasal chondrocytes (NCs) to modified gellan…

0301 basic medicineRegeneration (biology)Mesenchymal stem cellBiomedical EngineeringMedicine (miscellaneous)02 engineering and technology021001 nanoscience & nanotechnologyChondrogenesisIn vitroGellan gumCell biologyBiomaterials03 medical and health scienceschemistry.chemical_compound030104 developmental biologychemistryTissue engineeringIn vivoSelf-healing hydrogels0210 nano-technologyBiomedical engineeringJournal of Tissue Engineering and Regenerative Medicine
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Possible A2E Mutagenic Effects on RPE Mitochondrial DNA from Innovative RNA-Seq Bioinformatics Pipeline

2020

Mitochondria are subject to continuous oxidative stress stimuli that, over time, can impair their genome and lead to several pathologies, like retinal degenerations. Our main purpose was the identification of mtDNA variants that might be induced by intense oxidative stress determined by N-retinylidene-N-retinylethanolamine (A2E), together with molecular pathways involving the genes carrying them, possibly linked to retinal degeneration. We performed a variant analysis comparison between transcriptome profiles of human retinal pigment epithelial (RPE) cells exposed to A2E and untreated ones, hypothesizing that it might act as a mutagenic compound towards mtDNA. To optimize analysis, we propo…

0301 basic medicineRetinal degenerationMitochondrial DNAPhysiologyClinical BiochemistryMitochondrionBiologyBiochemistryGenomeArticle03 medical and health scienceschemistry.chemical_compound0302 clinical medicinemedicineRNA-SeqMolecular BiologyGeneGeneticsmtDNAlcsh:RM1-950RNACell Biologymedicine.diseasePhenotypeVUSmitochondrialcsh:Therapeutics. Pharmacology030104 developmental biologychemistrymitochondria mtDNA RNA-Seq retinal degenerations VUSretinal degenerationsAdenosine triphosphate030217 neurology & neurosurgeryAntioxidants
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The Absence of HIF-1α Increases Susceptibility to Leishmania donovani Infection via Activation of BNIP3/mTOR/SREBP-1c Axis

2020

Summary: Hypoxia-inducible factor-1 alpha (HIF-1α) is considered a global regulator of cellular metabolism and innate immune cell functions. Intracellular pathogens such as Leishmania have been reported to manipulate host cell metabolism. Herein, we demonstrate that myeloid cells from myeloid-restricted HIF-1α-deficient mice and individuals with loss-of-function HIF1A gene polymorphisms are more susceptible to L. donovani infection through increased lipogenesis. Absence of HIF-1α leads to a defect in BNIP3 expression, resulting in the activation of mTOR and nuclear translocation of SREBP-1c. We observed the induction of lipogenic gene transcripts, such as FASN, and lipid accumulation in inf…

0301 basic medicineSREBP-1cHIF1A Gene[SDV]Life Sciences [q-bio]Leishmania donovaniHIF-1αGeneral Biochemistry Genetics and Molecular BiologyMitochondrial Proteins03 medical and health sciences0302 clinical medicinevisceral leishmaniasisAnimalsHumansMyeloid Cellslcsh:QH301-705.5GenelipogenesisPI3K/AKT/mTOR pathwayDisease ResistanceMice Inbred BALB CInnate immune systembiologyIntracellular parasiteLipogenesisMacrophagesTOR Serine-Threonine KinasesGenetic VariationMembrane Proteinsbiology.organism_classificationLeishmaniaHypoxia-Inducible Factor 1 alpha SubunitFASNLipidsmacrophages3. Good healthCell biologyUp-RegulationMice Inbred C57BL030104 developmental biologylcsh:Biology (General)myeloid cellsLipogenesisLeishmaniasis VisceralDisease SusceptibilityacetateSterol Regulatory Element Binding Protein 1030217 neurology & neurosurgeryLeishmania donovaniSignal Transduction
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The cellular growth rate controls overall mRNA turnover, and modulates either transcription or degradation rates of particular gene regulons

2015

We analyzed 80 different genomic experiments, and found a positive correlation between both RNA polymerase II transcription and mRNA degradation with growth rates in yeast. Thus, in spite of the marked variation in mRNA turnover, the total mRNA concentration remained approximately constant. Some genes, however, regulated their mRNA concentration by uncoupling mRNA stability from the transcription rate. Ribosome-related genes modulated their transcription rates to increase mRNA levels under fast growth. In contrast, mitochondria-related and stress-induced genes lowered mRNA levels by reducing mRNA stability or the transcription rate, respectively. We also detected these regulations within th…

0301 basic medicineSaccharomyces cerevisiae ProteinsTranscription GeneticRNA StabilityPopulationRNA polymerase IIRNA-binding proteinSaccharomyces cerevisiaeChromatin and EpigeneticsRegulonGenètica molecular03 medical and health sciencesTranscripció genèticaTranscription (biology)GeneticsGene RegulationRNA MessengereducationGeneRegulation of gene expressionGeneticsMessenger RNAeducation.field_of_studyOrganelle BiogenesisbiologyGene regulation Chromatin and EpigeneticsRNA-Binding ProteinsRNAGenes rRNACell biologyGenes Mitochondrial030104 developmental biologyGene Expression Regulationbiology.proteinRNARibosomes
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Vascular ageing and endothelial cell senescence: Molecular mechanisms of physiology and diseases

2016

Ageing leads to a progressive deterioration of structure and function of all organs over the time. During this process endothelial cells undergo senescence and manifest significant changes in their properties, resulting in impairment of the vascular functionality and neo-angiogenic capability. This ageing-dependent impairment of endothelial functions is considered a key factor contributing to vascular dysfunctions, which is responsible of several age-related diseases of the vascular system and other organs. Several mechanisms have been described to control ageing-related endothelial cell senescence including microRNAs, mitochondrial dysfunction and micro environmental stressors, such as hyp…

0301 basic medicineSenescenceAgingEndotheliump73Biologymedicine.disease_cause03 medical and health sciencesEndotheliocyte; Endothelium; Hypoxia; MicroRNAs; Mitochondrial dysfunction; Oxidative stress; P53 family; P73; Transglutaminase 2; VEGF; Aging; Developmental BiologymicroRNAmedicineAnimalsHumansSettore MED/05 - Patologia ClinicaEndotheliocyte; Endothelium; Hypoxia; Mitochondrial dysfunction; Oxidative stress; Transglutaminase 2; VEGF; microRNAs; p53 family; p73Vascular DiseasesEndotheliumHypoxiaCellular SenescenceEndothelial CellsMicroRNASettore MED/23 - Chirurgia CardiacaBECN1Hypoxia (medical)VEGFMitochondriamicroRNAsEndothelial stem cellTransglutaminase 2030104 developmental biologymedicine.anatomical_structureOxidative stressAgeingImmunologyOxidative stremedicine.symptomMitochondrial dysfunctionp53 familyEndotheliocyteNeuroscienceOxidative stressDevelopmental BiologyMechanisms of Ageing and Development
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Paracrine effects of human adipose-derived mesenchymal stem cells in inflammatory stress-induced senescence features of osteoarthritic chondrocytes

2016

Aging and exposure to stress would determine the chondrocyte phenotype in osteoarthritis (OA). In particular, chronic inflammation may contribute to stress-induced senescence of chondrocytes and cartilage degeneration during OA progression. Recent studies have shown that adipose-derived mesenchymal stem cells exert paracrine effects protecting against degenerative changes in chondrocytes. We have investigated whether the conditioned medium (CM) from adipose-derived mesenchymal stem cells may regulate senescence features induced by inflammatory stress in OA chondrocytes. Our results indicate that CM down-regulated senescence markers induced by interleukin-1β including senescence-associated β…

0301 basic medicineSenescenceAgingPathologymedicine.medical_specialtyadipose-derived mesenchymal stem cells conditioned mediumsenescenceCaveolin 1chondrocytesAdipose tissueInflammationmedicine.disease_cause03 medical and health sciencesParacrine signalling0302 clinical medicineOsteoarthritisParacrine CommunicationmedicineHumansCellular SenescenceInflammation030203 arthritis & rheumatologybiologySirtuin 1KinaseMesenchymal stem cellMesenchymal Stem CellsCell Biologybeta-GalactosidaseCell biologyOxidative Stress030104 developmental biologyAdipose Tissuebiology.proteinmedicine.symptomOxidative stressResearch PaperAging
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