Search results for "Gene Expression Regulation"

showing 10 items of 2328 documents

The close link between the fetal programming imprinting and neurodegeneration in adulthood: The key role of “hemogenic endothelium” programming

2021

The research on neurodegenerative diseases (NeuroDegD) has been traditionally focused on later life stages. There is now an increasing evidence, that they may be programmed during early development. Here, we propose that NeuroDegD are the result of the complex process of imprinting on fetal hemogenic endothelium, from which the microglial cells make to origin. The central role of placenta and epigenetic mechanisms (methylation of DNA, histone modifications and regulation by non-coding RNAs) in mediating the short and long-term effects has been also described. Precisely, it reports their role in impacting plasticity and memory of microglial cells. In addition, we also underline the necessity…

0301 basic medicineAgingHemangioblastsCell PlasticityRisk AssessmentEpigenesis GeneticFetal DevelopmentMolecular Imprinting03 medical and health sciences0302 clinical medicineEpigenetic factors as biomarkers Sex dimorphism Fetal developmental programming Hemogenic endothelium Microglia plasticity and memory Neurodegenerative diseasesmedicineHumansSettore MED/05 - Patologia ClinicaEpigeneticsFetal programmingImprinting (organizational theory)Hemogenic endotheliumSex CharacteristicsBiological Variation Individualbiologybusiness.industryNeurodegenerationGene Expression Regulation DevelopmentalNeurodegenerative Diseasesmedicine.diseaseLife stage030104 developmental biologyHistonePrenatal stressbiology.proteinMicrogliabusinessNeuroscienceBiomarkers030217 neurology & neurosurgeryDevelopmental BiologyMechanisms of Ageing and Development
researchProduct

Intensified mitophagy in skeletal muscle with aging is downregulated by PGC-1alpha overexpression in vivo.

2018

Mitochondrial dysfunction plays an important role in the etiology of age-related muscle atrophy known as sarcopenia. PGC-1α is positioned at the center of crosstalk in regulating mitochondrial quality control, but its role in mitophagy in aged skeletal muscle is currently unclear. The present study investigated the effects of aging and PGC-1α overexpression via in vivo DNA transfection on key mitophagy protein markers, as well as mitochondrial dynamics related proteins, metabolic function and antioxidant capacity in mouse muscle. C57BL/6J mice at the age of 2 mo (young, Y; N = 14) and 24 mo (old, O; N = 14) were transfected in vivo with either PGC-1α DNA (OE, N = 7) or GFP (N = 7) into the …

0301 basic medicineAgingUbiquitin-Protein LigasesPINK1MitochondrionBiochemistryMitochondrial DynamicsGTP Phosphohydrolases03 medical and health sciencesMice0302 clinical medicineIn vivoPhysiology (medical)MitophagymedicineAnimalsMuscle SkeletalChemistryMitophagySkeletal muscleTransfectionmedicine.diseasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaMuscle atrophyCell biologyMitochondriaOxidative Stress030104 developmental biologymedicine.anatomical_structureGene Expression RegulationSarcopeniaBeclin-1medicine.symptomProtein Kinases030217 neurology & neurosurgeryFree radical biologymedicine
researchProduct

A novel microglial subset plays a key role in myelinogenesis in developing brain.

2017

Microglia are resident macrophages of the central nervous system that contribute to homeostasis and neuroinflammation. Although known to play an important role in brain development, their exact function has not been fully described. Here, we show that in contrast to healthy adult and inflammation-activated cells, neonatal microglia show a unique myelinogenic and neurogenic phenotype. A CD11c(+) microglial subset that predominates in primary myelinating areas of the developing brain expresses genes for neuronal and glial survival, migration, and differentiation. These cells are the major source of insulin-like growth factor 1, and its selective depletion from CD11c(+) microglia leads to impa…

0301 basic medicineAgingmedicine.medical_treatmentNews & ViewsInsulin-Like Growth Factor IMyelin SheathCell AggregationNeural PlateMicrogliaACTIVATED MICROGLIAGeneral NeuroscienceExperimental autoimmune encephalomyelitisNeurogenesisIGF1BrainGene Expression Regulation DevelopmentalADULT BRAINUp-RegulationALZHEIMERS-DISEASEmedicine.anatomical_structureEXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITISMyelinogenesisGROWTHFemaleMicrogliaCNSEncephalomyelitis Autoimmune ExperimentalNeurogenesisCentral nervous systemCD11cBiologyGeneral Biochemistry Genetics and Molecular BiologyDEPENDENT MANNER03 medical and health sciencesmedicinePOSTNATAL-DEVELOPMENTAnimalsMolecular BiologyNeuroinflammationGeneral Immunology and MicrobiologyCD11cGrowth factorGene Expression ProfilingCENTRAL-NERVOUS-SYSTEMmedicine.diseaseGALECTIN-1CD11c AntigenMice Inbred C57BL030104 developmental biologynervous systemAnimals NewbornImmunologymyelinogenesisNeuroscienceBiomarkersThe EMBO journal
researchProduct

Estradiol, acting through ERα, induces endothelial non-classic renin-angiotensin system increasing angiotensin 1–7 production

2016

Intracellular renin-angiotensin system (RAS) can operate independently of the circulating RAS. Estrogens provide protective effects by modulating the RAS. Our aim was to investigate the effect of estradiol (E2) on angiotensin converting enzymes (ACE) 1 and ACE2 expression and activities in human endothelial cells (HUVEC), and the role of estrogen receptors (ER). The results confirmed the presence of active intracellular RAS in HUVEC. Physiological concentrations of E2 induced a concentration-dependent increase of ACE1 and ACE2 mRNA expression and ACE1, but not ACE2, protein levels. ACE1 and ACE2 enzymatic activities were also induced with E2. These effects were mediated through ERα activati…

0301 basic medicineAgonistmedicine.medical_specialtymedicine.drug_classEstrogen receptorPeptidyl-Dipeptidase A030204 cardiovascular system & hematologyBiologyBiochemistryEstrogen Receptor AntagonistsCiencias Biológicas03 medical and health sciences0302 clinical medicineEndocrinologyPiperidinesInternal medicineRenin–angiotensin systemHuman Umbilical Vein Endothelial CellsmedicineHumansFulvestrantMolecular BiologyESTROGEN RECEPTORDose-Response Relationship DrugEstradiolEstrogen Receptor alphaANGIOTENSIN CONVERTING ENZYMESBioquímica y Biología MolecularRENIN ANGIOTENSIN SYSTEMPeptide FragmentsEndothelial stem cellESTROGEN030104 developmental biologyEndocrinologyGene Expression RegulationEstrogenENDOTHELIAL CELLPyrazolesAngiotensin-Converting Enzyme 2Estrogen Receptor AntagonistsAngiotensin IEstrogen receptor alphaCIENCIAS NATURALES Y EXACTAShormones hormone substitutes and hormone antagonistsIntracellularMolecular and Cellular Endocrinology
researchProduct

Distinctive Histogenesis and Immunological Microenvironment Based on Transcriptional Profiles of Follicular Dendritic Cell Sarcomas

2017

Abstract Follicular dendritic cell (FDC) sarcomas are rare mesenchymal tumors with variable clinical, morphologic, and phenotypic characteristics. Transcriptome analysis was performed on multiple FDC sarcomas and compared with other mesenchymal tumors, microdissected Castleman FDCs, and normal fibroblasts. Using unsupervised analysis, FDC sarcomas clustered with microdissected FDCs, distinct from other mesenchymal tumors and fibroblasts. The specific endowment of FDC-related gene expression programs in FDC sarcomas emerged by applying a gene signature of differentially expressed genes (n = 1,289) between microdissected FDCs and fibroblasts. Supervised analysis comparing FDC sarcomas with mi…

0301 basic medicineAlgorithms; B7-H1 Antigen; Castleman Disease; Chromatin; Cluster Analysis; Dendritic Cell Sarcoma Follicular; Gene Expression Profiling; Gene Expression Regulation Neoplastic; Humans; Programmed Cell Death 1 Ligand 2 Protein; Programmed Cell Death 1 Receptor; Signal Transduction; T-Lymphocytes Helper-Inducer; T-Lymphocytes Regulatory; Up-Regulation; Gene Regulatory Networks; Molecular Biology; Oncology; Cancer ResearchCancer ResearchProgrammed Cell Death 1 ReceptorDendritic Cell Sarcoma FollicularBiologyT-Lymphocytes RegulatoryB7-H1 AntigenTranscriptome03 medical and health sciencesmedicineCluster AnalysisHumansGene Regulatory NetworksMolecular BiologyRegulation of gene expressionCluster AnalysiGene Regulatory NetworkFollicular dendritic cellsCastleman DiseaseGene Expression ProfilingMesenchymal stem cellT-Lymphocytes Helper-InducerProgrammed Cell Death 1 Ligand 2 Proteinmedicine.diseaseChromatinUp-RegulationAlgorithmGene Expression Regulation NeoplasticGene expression profiling030104 developmental biologyOncologyCancer researchImmunohistochemistrySarcomaAlgorithmsHumanSignal TransductionExtracellular matrix organizationMolecular Cancer Research
researchProduct

Expression of Alpha-Enolase (ENO1), Myc Promoter-Binding Protein-1 (MBP-1) and Matrix Metalloproteinases (MMP-2 and MMP-9) Reflect the Nature and Agg…

2019

Breast cancer is a complex and heterogeneous disease: Several molecular alterations cause cell proliferation and the acquisition of an invasive phenotype. Extracellular matrix (ECM) is considered essential for sustaining tumor growth and matrix metalloproteinases (MMPs) have been identified as drivers of many aspects of the tumor phenotype. Mounting evidence indicates that both &alpha

0301 basic medicineAlpha-enolaseENO1Kaplan-Meier EstimateMatrix metalloproteinasemedicine.disease_causeMetastasisExtracellular matrixlcsh:Chemistry0302 clinical medicineSettore BIO/06 - Anatomia Comparata E Citologialcsh:QH301-705.5SpectroscopybiologyMMP-2General MedicineComputer Science ApplicationsDNA-Binding ProteinsGene Expression Regulation NeoplasticMatrix Metalloproteinase 9030220 oncology & carcinogenesisDisease ProgressionMatrix Metalloproteinase 2FemaleMMP-9Breast NeoplasmsCatalysisArticleInorganic Chemistry03 medical and health sciencesBreast cancerbreast cancerCell Line TumormedicineBiomarkers TumorHumansPhysical and Theoretical ChemistryMBP-1Molecular BiologyCell ProliferationTumor Suppressor ProteinsOrganic ChemistryCancermedicine.diseaseSettore BIO/18 - Genetica030104 developmental biologylcsh:Biology (General)lcsh:QD1-999Phosphopyruvate HydrataseCancer cellbiology.proteinCancer researchCarcinogenesisInternational Journal of Molecular Sciences
researchProduct

Tocotrienol Affects Oxidative Stress, Cholesterol Homeostasis and the Amyloidogenic Pathway in Neuroblastoma Cells: Consequences for Alzheimer’s Dise…

2016

One of the characteristics of Alzheimer´s disease (AD) is an increased amyloid load and an enhanced level of reactive oxidative species (ROS). Vitamin E has known beneficial neuroprotective effects, and previously, some studies suggested that vitamin E is associated with a reduced risk of AD due to its antioxidative properties. However, epidemiological studies and nutritional approaches of vitamin E treatment are controversial. Here, we investigate the effect of α-tocotrienol, which belongs to the group of vitamin E, on AD-relevant processes in neuronal cell lines. In line with the literature, α-tocotrienol reduced the ROS level in SH-SY5Y cells. In the presence of tocotrienols, cholesterol…

0301 basic medicineAlzheimer´s diseasemedicine.medical_treatmentvitamin Eγ-secretasemedicine.disease_causeAntioxidantslcsh:ChemistryNeuroblastomachemistry.chemical_compoundAβ degradation0302 clinical medicineβ-secretaselcsh:QH301-705.5SpectroscopyNeuronschemistry.chemical_classificationbiologyTocotrienolsGeneral Medicinetocopherol3. Good healthComputer Science ApplicationsCholesterolNeuroprotective AgentsTocotrienolmedicine.medical_specialtyAmyloidamyloid-βNeuroprotectionArticleGene Expression Regulation EnzymologicCatalysisCell LineInorganic Chemistry03 medical and health sciencesAlzheimer DiseaseInternal medicinemedicineHumanstocotrienolPhysical and Theoretical ChemistryMolecular BiologyReactive oxygen speciesAmyloid beta-PeptidesCholesterolVitamin EOrganic Chemistrytocotrienol; vitamin E; Alzheimer´s disease; amyloid-β; tocopherol; Aβ degradation; β-secretase; γ-secretaseOxidative Stress030104 developmental biologyEndocrinologychemistrylcsh:Biology (General)lcsh:QD1-999biology.proteinAmyloid Precursor Protein SecretasesReactive Oxygen SpeciesAmyloid precursor protein secretase030217 neurology & neurosurgeryOxidative stressInternational Journal of Molecular Sciences
researchProduct

Direct Sensing of Nutrients via a LAT1-like Transporter in Drosophila Insulin-Producing Cells

2016

Summary Dietary leucine has been suspected to play an important role in insulin release, a hormone that controls satiety and metabolism. The mechanism by which insulin-producing cells (IPCs) sense leucine and regulate insulin secretion is still poorly understood. In Drosophila, insulin-like peptides (DILP2 and DILP5) are produced by brain IPCs and are released in the hemolymph after leucine ingestion. Using Ca2+-imaging and ex vivo cultured larval brains, we demonstrate that IPCs can directly sense extracellular leucine levels via minidiscs (MND), a leucine transporter. MND knockdown in IPCs abolished leucine-dependent changes, including loss of DILP2 and DILP5 in IPC bodies, consistent wit…

0301 basic medicineAmino Acid Transport Systemsheavy-chainmedicine.medical_treatmentInsulinsamino acid transporter0302 clinical medicinegenetics [Drosophila Proteins]cytology [Drosophila melanogaster]Glutamate DehydrogenaseHemolymphInsulin-Secreting Cellsmetabolism [Drosophila melanogaster]HemolymphDrosophila;Drosophila insulin-like peptides;amino acid transporter;food;glutamate dehydrogenase;glycemia;growth;insulin-producing cells;minidiscs;starvationDrosophila ProteinsProtein Isoformsmetabolism [Calcium]genetics [Insulins]genetics [Amino Acid Transport Systems]lcsh:QH301-705.5minidiscsGene knockdowncytology [Larva]pancreatic beta-cellglutamate dehydrogenaseBrainmetabolism [Hemolymph]secretionDrosophila melanogasterBiochemistryLarvaAlimentation et NutritionDrosophilaLeucineSignal Transductionglucose-transportgenetics [Glutamate Dehydrogenase]genetics [Protein Isoforms]growthamino-acidsmetabolism [Drosophila Proteins][SDV.BC]Life Sciences [q-bio]/Cellular BiologyNutrient sensingmetabolism [Larva]Biologyinsulin-producing cellsArticleGeneral Biochemistry Genetics and Molecular Biologymetabolism [Amino Acid Transport Systems]metabolism [Insulins]03 medical and health sciencesLeucineparasitic diseasesmedicineFood and NutritionAnimalsddc:610cytology [Insulin-Secreting Cells]cardiovascular diseasesAmino acid transporterMnd protein Drosophilaadministration & dosage [Leucine]metabolism [Protein Isoforms]Ilp5 protein Drosophilacytology [Brain]foodGlutamate dehydrogenaseInsulinNeurosciencesstarvationGlucose transportermetabolism [Insulin-Secreting Cells]glutamate-dehydrogenasel-leucineglycemia030104 developmental biologyGene Expression Regulationlcsh:Biology (General)metabolism [Brain]metabolism [Glutamate Dehydrogenase]Neurons and Cognitionmetabolism [Leucine]CalciumDrosophila insulin-like peptidesmetabolismfat-cells030217 neurology & neurosurgeryCell Reports
researchProduct

DNA demethylation caused By 5-Aza-2'-Deoxycytidine induces mitotic alterations and aneuploidy

2016

Aneuploidy, the unbalanced number of chromosomes in a cell, is considered a prevalent form of genetic instability and is largely acknowledged as a condition implicated in tumorigenesis. Epigenetic alterations like DNA hypomethylation have been correlated with cancer initiation/progression. Furthermore, a growing body of evidence suggests the involvement of epigenome-wide disruption as a cause of global DNA hypomethylation in aneuploidy generation. Here, we report that the DNA hypomethylating drug 5-aza-2′-deoxycytidine (DAC), affects the correct ploidy of nearly diploid HCT-116 human cells by altering the methylation pattern of the chromosomes. Specifically, we show that a DAC-induced reduc…

0301 basic medicineAntimetabolites Antineoplastic5-aza-2'-deoxycytidine (DAC); Aneuploidy; Chromosome methylation pattern; Chromosome Section; DNA demethylation; OncologyBlotting WesternAneuploidyMitosisApoptosisBiologymedicine.disease_causeDecitabineReal-Time Polymerase Chain ReactionChromosome Section03 medical and health scienceschromosome methylation patternChromosome instabilitymedicineTumor Cells CulturedHumansEpigeneticsaneuploidyRNA Messenger5-aza-2′-deoxycytidine (DAC)Cell ProliferationGeneticsChromosome AberrationsPloidiesReverse Transcriptase Polymerase Chain ReactionDNA Methylationmedicine.disease5-aza-2'-deoxycytidine (DAC)Gene Expression Regulation NeoplasticResearch Paper: ChromosomeSettore BIO/18 - Genetica030104 developmental biologyDNA demethylationOncologyMicroscopy FluorescenceDNA methylationColonic NeoplasmsCytogenetic AnalysisCancer researchDNA demethylationAzacitidinePloidyCarcinogenesisDNA hypomethylation
researchProduct

Pinolenic acid ameliorates oleic acid-induced lipogenesis and oxidative stress via AMPK/SIRT1 signaling pathway in HepG2 cells

2019

Pinolenic acid (PLA), a natural compound isolated from pine nut oil, has been reported to exert bioactivity against lipid anabolism. Nonetheless, the underlying mechanisms still poorly elucidated. The aim of this study is to comprehensively demonstrate the effects of PLA on oleic acid (OA)-induced non-alcoholic fatty liver disease (NAFLD) and their relationship with the lipid metabolic regulation. The results demonstrated that treatment with PLA dramatically inhibited lipid accumulation, oxidative stress as well as inflammatory responses induced by oleic acid in HepG2 cells. PLA also obviously decreased the levels of cellular triglyceride (TG), total cholesterol (TC), malondialdehyde (MDA),…

0301 basic medicineAntioxidantLinolenic Acidsmedicine.medical_treatmentPinolenic acidAMP-Activated Protein KinasesNitric Oxidemedicine.disease_causePine nut oil03 medical and health scienceschemistry.chemical_compound0302 clinical medicineSirtuin 1medicineHumansPPAR alphaPharmacologybiologyLipogenesisAMPKHep G2 CellsOxidative StressFatty acid synthaseOleic acid030104 developmental biologyGene Expression RegulationchemistryBiochemistryLipogenesisbiology.proteinlipids (amino acids peptides and proteins)030217 neurology & neurosurgeryOxidative stressOleic AcidSignal TransductionEuropean Journal of Pharmacology
researchProduct