Search results for "Granulocyte Precursor Cells"

showing 3 items of 3 documents

Differential expression of specific microRNA and their targets in acute myeloid leukemia

2010

Acute myeloid leukemia (AML) the most common acute leukemia in adults is characterized by various cytogenetic and molecular abnormalities. However, the genetic etiology of the disease is not yet fully understood. MicroRNAs (miRNA) are small noncoding RNAs which regulate the expression of target mRNAs both at transcriptional and translational level. In recent years, miRNAs have been identified as a novel mechanism in gene regulation, which show variable expression during myeloid differentiation. We studied miRNA expression of leukemic blasts of 29 cases of newly diagnosed and genetically defined AML using quantitative reverse transcription polymerase chain reaction (RT-PCR) for 365 human miR…

AdultMaleNPM1Down-RegulationBiologySettore MED/15 - Malattie Del SangueYoung Adulthemic and lymphatic diseasesmicroRNAmedicineGene silencingHumansLeukemia microarray data microRNAGranulocyte Precursor CellsAgedCell ProliferationGeneticsRegulation of gene expressionAged 80 and overAcute leukemiaReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingCore Binding FactorsMyeloid leukemiaNuclear ProteinsCell DifferentiationHematologyMiddle Agedmedicine.diseaseUp-RegulationGene expression profilingGene Expression Regulation NeoplasticLeukemiaLeukemia Myeloid AcuteMicroRNAsfms-Like Tyrosine Kinase 3Case-Control StudiesMutationFemaleSettore SECS-S/01 - StatisticaNucleophosmin
researchProduct

The hematopoietic factor G-CSF is a neuronal ligand that counteracts programmed cell death and drives neurogenesis.

2005

G-CSF is a potent hematopoietic factor that enhances survival and drives differentiation of myeloid lineage cells, resulting in the generation of neutrophilic granulocytes. Here, we show that G-CSF passes the intact blood-brain barrier and reduces infarct volume in 2 different rat models of acute stroke. G-CSF displays strong anti-apoptotic activity in mature neurons and activates multiple cell survival pathways. Both G-CSF and its receptor are widely expressed by neurons in the CNS, and their expression is induced by ischemia, which suggests an autocrine protective signaling mechanism. Surprisingly, the G-CSF receptor was also expressed by adult neural stem cells, and G-CSF induced neurona…

Malemedicine.medical_specialtyProgrammed cell deathNeutrophilsCellular differentiationApoptosisBiologyLigandsBrain IschemiaBrain ischemiaInternal medicineGranulocyte Colony-Stimulating FactormedicineAnimalsHumansGranulocyte Precursor CellsNerve TissueRats WistarReceptorAutocrine signallingStem CellsNeurogenesisCell DifferentiationNeurodegenerative DiseasesGeneral Medicinemedicine.diseaseNeural stem cellCell biologyRatsStrokeDisease Models AnimalEndocrinologyBlood-Brain BarrierReceptors Granulocyte Colony-Stimulating FactorStem cellResearch ArticleThe Journal of clinical investigation
researchProduct

Steady-state neutrophil homeostasis is dependent on TLR4/TRIF signaling

2013

Polymorphonuclear neutrophil granulocytes (neutrophils) are tightly controlled by an incompletely understood homeostatic feedback loop adjusting the marrow's supply to peripheral needs. Although it has long been known that marrow cellularity is inversely correlated with G-CSF levels, the mechanism linking peripheral clearance to production remains unknown. Herein, the feedback response to antibody induced neutropenia is characterized to consist of G-CSF–dependent shifts of marrow hematopoietic progenitor populations including expansion of the lin-/Sca-1/c-kit (LSK) and granulocyte macrophage progenitor (GMP) compartments at the expense of thrombopoietic and red cell precursors. Evidence is …

NeutrophilsImmunologyRecombinant Granulocyte Colony-Stimulating FactorBiologyBiochemistryGranulopoiesisMiceGranulocyte Colony-Stimulating FactorAnimalsHomeostasisGranulocyte Precursor CellsLymphocytesNeutrophil homeostasisReceptorMice KnockoutCell BiologyHematologyGranulocyte colony-stimulating factorToll-Like Receptor 4Adaptor Proteins Vesicular TransportTRIFMyeloid Differentiation Factor 88ImmunologyTLR4HomeostasisSignal TransductionBlood
researchProduct