Search results for " Granulocyte Colony-Stimulating Factor"

showing 5 items of 5 documents

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
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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
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Mesenchymal Transition of High-Grade Breast Carcinomas Depends on Extracellular Matrix Control of Myeloid Suppressor Cell Activity

2016

SummaryThe extracellular matrix (ECM) contributes to the biological and clinical heterogeneity of breast cancer, and different prognostic groups can be identified according to specific ECM signatures. In high-grade, but not low-grade, tumors, an ECM signature characterized by high SPARC expression (ECM3) identifies tumors with increased epithelial-to-mesenchymal transition (EMT), reduced treatment response, and poor prognosis. To better understand how this ECM3 signature is contributing to tumorigenesis, we expressed SPARC in isogenic cell lines and found that SPARC overexpression in tumor cells reduces their growth rate and induces EMT. SPARC expression also results in the formation of a h…

0301 basic medicineMyeloidMDSCGene Expressionmedicine.disease_causeT-Lymphocytes RegulatoryPolyethylene GlycolsExtracellular matrixMiceBreast cancerMyeloid CellsOsteonectinMast Cellslcsh:QH301-705.5Mice KnockoutAntigen PresentationMice Inbred BALB CEMTepithelial to mesenchymal transitionBreast cancer; COX-2; CXCL12; ECM; EMT; G-CSF; GM-CSF; MDSC; SPARC; aminobisphosphonates; cyclooxygenase-2; epithelial to mesenchymal transition; extracellular matrix; granulocyte colony-stimulating factor; granulocyte-macrophage colony-stimulating factor; myeloid-derived suppressor cellsCXCL12Granulocyte macrophage colony-stimulating factormedicine.anatomical_structurecyclooxygenase-2granulocyte-macrophage colony-stimulating factorFemalegranulocyte colony-stimulating factormedicine.drugEpithelial-Mesenchymal Transitionextracellular matrixAntineoplastic AgentsBreast NeoplasmsBiologySettore MED/08 - Anatomia PatologicaG-CSFGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesCell Line TumormedicineAnimalsHumansEpithelial–mesenchymal transitionECMMesenchymal stem cellSPARCGM-CSFCOX-2myeloid-derived suppressor cellsXenograft Model Antitumor AssaysIsogenic human disease modelsaminobisphosphonates030104 developmental biologylcsh:Biology (General)CelecoxibDoxorubicinImmunologyCancer researchMyeloid-derived Suppressor CellaminobisphosphonateNeoplasm GradingCarcinogenesisCell Reports
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Neuroprotective effect of Fn14 deficiency is associated with induction of the granulocyte-colony stimulating factor (G-CSF) pathway in experimental s…

2010

Using a transgenic mouse model of ischemic stroke we checked for a possible interaction of antiphospholipid antibodies (aPL) which often cause thromboses as well as central nervous system (CNS) involvement under non-thrombotic conditions and the TWEAK/Fn14 pathway known to be adversely involved in inflammatory and ischemic brain disease. After 7 days, infarct volumes were reduced in Fn14 deficient mice and were further decreased by aPL treatment. This was associated with strongest increase of the endogenous neuroprotective G-CSF/G-CSF receptor system. This unexpected beneficial action of aPL is an example for a non-thrombogenic action and the double-edged nature of aPL.

MaleGenetically modified mouseImmunologyMice TransgenicBiologyNeuroprotectionReceptors Tumor Necrosis FactorBrain IschemiaMiceRandom AllocationTissue factorimmune system diseasesAntiphospholipid syndromeGranulocyte Colony-Stimulating FactormedicineAnimalsHumansImmunology and AllergyneoplasmsStrokeLupus anticoagulantmedicine.diseaseMice Inbred C57BLDisease Models AnimalNeurologyTWEAK ReceptorReceptors Granulocyte Colony-Stimulating FactorImmunologyAntibodies AntiphospholipidTumor necrosis factor alphaNeurology (clinical)Inflammation MediatorsGranulocyte colony-stimulating factor receptorSignal TransductionJournal of Neuroimmunology
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Distribution of the hematopoietic growth factor G-CSF and its receptor in the adult human brain with specific reference to Alzheimer's disease

2013

The granulocyte colony-stimulating factor (G-CSF), being a member of the hematopoietic growth factor family, is also critically involved in controlling proliferation and differentiation of neural stem cells. Treatment with G-CSF has been shown to result in substantial neuroprotective and neuroregenerative effects in various experimental models of acute and chronic diseases of the central nervous system. Although G-CSF has been tested in a clinical study for treatment of acute ischemic stroke, there is only fragmentary data on the distribution of this cytokine and its receptor in the human brain. Therefore, the present study was focused on the immunohistochemical analysis of the protein expr…

MaleHistologyHematopoietic growth factorCentral nervous systemNeuroprotectionAlzheimer DiseaseGranulocyte Colony-Stimulating FactormedicineHumansMolecular BiologyEcology Evolution Behavior and SystematicsAgedAged 80 and overNeuronsbiologyBrainOriginal ArticlesCell BiologyHuman brainMiddle AgedImmunohistochemistryNeural stem cellmedicine.anatomical_structureCase-Control StudiesReceptors Granulocyte Colony-Stimulating FactorImmunologybiology.proteinFemaleChoroid plexusAnatomyGranulocyte colony-stimulating factor receptorNeuroscienceDevelopmental BiologyNeurotrophinJournal of Anatomy
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