Search results for "Bone Marrow"

showing 10 items of 538 documents

Cdc42 in osterix-expressing cells alters osteoblast behavior and myeloid lineage commitment

2021

Osteoblasts are not only responsible for bone formation. They also support hematopoiesis. This requires responding to cues originating from several signaling pathways, a task performed by Rho GTPases. We therefore examined several transgenic mouse models and used inhibitors of Cdc42 in vitro. Deletion of Cdc42 in vivo using the Osterix promoter suppressed osteoblast function, while its deletion in differentiating osteoblasts using the Collagen-a1(I) promoter decreased osteoblast numbers. In both cases, bone mineral density diminished confirming the importance of Cdc42. Evaluation of hematopoiesis revealed that deletion of Cdc42 using the Osterix, but not the Collagen-a1(I) promoter increase…

Genetically modified mousemusculoskeletal diseasesOsteoblastsHistologyMyeloidStromal cellPhysiologyChemistryEndocrinology Diabetes and MetabolismCell DifferentiationOsteoblastmacromolecular substancesBone and BonesCell biologyMiceHaematopoiesismedicine.anatomical_structureOsteogenesismedicineAnimalsCell LineageMyelopoiesisBone marrowSignal transduction
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C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation

2015

Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa−/−) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa−/− mi…

Genetics and Molecular Biology (all)0301 basic medicinePROTEINGeneral Physics and AstronomyMELANOMAApoptosisInbred C57BLBiochemistryDISEASEAnimals; Apoptosis; Cell Line Tumor; Cell Movement; Cell Proliferation; Complement Activation; Complement C1q; Complement C3; Complement C5; Humans; Mice; Mice Inbred C57BL; Mice Knockout; Neoplasms; Biochemistry Genetics and Molecular Biology (all); Chemistry (all); Physics and Astronomy (all)Micefluids and secretionsCell Movementimmune system diseasesNeoplasmsIMMUNE-RESPONSEskin and connective tissue diseasesComplement ActivationComplement C1qMice KnockoutComplement component 5TumorMultidisciplinaryQChemistry (all)Complement C5Complement C33. Good healthCell biologyMultidisciplinary SciencesDEFICIENCYmedicine.anatomical_structureScience & Technology - Other TopicsHumanKnockoutSciencechemical and pharmacologic phenomenaBiologyArticleGeneral Biochemistry Genetics and Molecular BiologyTROPHOBLAST INVASIONMECHANISMSCell LinePhysics and Astronomy (all)03 medical and health sciencesClassical complement pathwayImmune systemINFLAMMATIONCell Line TumormedicineAnimalsHumansCell ProliferationScience & TechnologyBiochemistry Genetics and Molecular Biology (all)AnimalCell growthEFFECTOR SYSTEMComplement C1qApoptosiGeneral ChemistryComplement systemMice Inbred C57BL030104 developmental biologyCancer cellNeoplasmBone marrowANTIBODY THERAPYNature Communications
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Editorial: Genetics and gene therapy of lysosomial storage disorders

2018

Non applicabile in quanto editoriale

Geneticsbusiness.industryAnimalGenetic enhancementGenetic TherapyLysosomeLysosomal Storage DiseasesDisease Models AnimalLysosomal Storage DiseaseDrug DiscoveryGeneticsAnimalsHumansMolecular MedicineMedicineEnzyme Replacement TherapyLysosomesbusinessMolecular BiologyGenetics (clinical)Bone Marrow TransplantationHuman
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Cytomegalovirus inhibits the engraftment of donor bone marrow cells by downregulation of hemopoietin gene expression in recipient stroma

1998

ABSTRACT Cytomegalovirus (CMV) disease after bone marrow (BM) transplantation is often associated with BM graft failure. There are two possible reasons for such a correlation. First, a poor hematopoietic reconstitution of unrelated etiology could promote the progression of CMV infection by the lack of immune control. Alternatively, CMV infection could interfere with the engraftment of donor BM cells in recipient BM stroma. Evidence for a causative role of CMV in BM aplasia came from studies in long-term BM cultures and from the murine in vivo model of CMV-induced aplastic anemia. A deficiency in the expression of essential stromal hemopoietins, such as stem cell factor (SCF), has indicated …

Graft RejectionMaleStromal cellImmunologyPopulationCytomegalovirusDown-RegulationViral Pathogenesis and ImmunityStem cell factorBiologyHematopoietic Cell Growth FactorsMicrobiologyMiceVirologymedicineAnimalsAplastic anemiaeducationBone Marrow Transplantationeducation.field_of_studyMice Inbred BALB CHematopoietic Cell Growth Factorsmedicine.diseaseTransplantationHaematopoiesisTransplantation Isogeneicmedicine.anatomical_structureInsect ScienceImmunologyCytomegalovirus InfectionsFemaleBone marrowStromal Cells
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Can bone marrow-derived multipotent adult progenitor cells regenerate infarcted myocardium?

2006

Objectives: To assess the functional effects of multipotent adult progenitor cells (MAPCs) transplanted in a rat model of chronic myocardial infarction. Methods: Forty-four rats underwent coronary ligation and, 14 days later, were randomly allocated to receive in-scar injections (5×106 cells/150 μL) of green fluorescent protein (eGFP)-transduced allogeneic MAPCs ( n =25) or culture medium (controls, n =19). Nine of the MAPC-treated hearts were employed for functional studies while the remaining 16 received cells co-labeled with Resovist™ and were only used for serial histological assessments. Left ventricular (LV) function was assessed echocardiographically before transplantation and 1 mont…

Graft RejectionPathologymedicine.medical_specialtyEndotheliumPhysiologyMyocardial InfarctionBone Marrow CellsRats Sprague-DawleyPhysiology (medical)MedicineAnimalsMyocardial infarctionTreatment FailureProgenitor cellbusiness.industryMultipotent Stem CellsMyocardiummedicine.diseaseMyocardial ContractionRatsTransplantationmedicine.anatomical_structureMultipotent Stem CellModels AnimalImmunohistochemistryFemaleBone marrowStem cellCardiology and Cardiovascular MedicinebusinessCardiovascular research
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Die Entwicklung der Myelofibrose bei der "präfibrotischen"cIMF

2002

Zusammenfassung Wegen des erst kurzlich mit Erscheinen der neuen WHO-Klassifikation der chronischen myeloproliferativen Erkrankungen (CMPE) aufgegebenen Festhaltens an einer Knochenmarksfibrose als wesentliches Merkmal der chronischen idiopathischen Myelofibrose (cIMF) sind Verlaufsuntersuchungen zu der Entwicklung einer Myelofibrose (MF) bei dieser Entitat nur von fibrotischen Stadien mit widerspruchlichen Ergebnissen bekannt. Deshalb wurde eine retrospektive Studie an Verlaufsbiopsien von 38 Patienten mit cIMF ohne initiale Fibrose mit der Frage nach der Haufigkeit, der Geschwindigkeit sowie dem Ausmas der Entwicklung einer MF durchgefuhrt. Unabhangig von einer Chemotherapie fanden wir ei…

Gynecologymedicine.medical_specialtymedicine.anatomical_structurebusiness.industryDisease progressionmedicineBone marrowbusinessMyelofibrosismedicine.diseasePathology and Forensic MedicineDer Pathologe
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Chromosomenuntersuchungen aus Lymphocyten und Knochenmark von Psoriasis-Kranken nach Langzeitbehandlung mit Methotrexat

1970

4 Psoriasis-Patienten, 3 davon mit zuruckliegender Arsenexposition, hatten Gesamtmengen zwischen 570 und 2735 mg Methotrexat erhalten. Bei diesen Patienten wurden Chromosomendarstellungen aus dem Knochenmark und aus Lymphocytenkulturen durchgefuhrt. Im Knochenmark (ohne Kultur in vitro) fanden sich keine eindeutigen Aberrationen, wahrend in den Lymphocyten in 2 Fallen gehauft (24%) ein Chromosom regellos fehlte, und bei einem Patienten einzelne Bruche zu finden waren. Soweit aus diesen Beobachtungen in Verbindung mit den Daten der Literatur Schlusse gezogen werden durfen, werden sie bezuglich der Chromosomenmutationen diskutiert.

Gynecologymedicine.medical_specialtymedicine.anatomical_structurebusiness.industrymedicineChromosomeMethotrexateDermatologyGeneral MedicineBone marrowbusinessmedicine.drugArchiv f�r Klinische und Experimentelle Dermatologie
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Contact Sensitizers Specifically Increase MHC Class II Expression on Murine Immature Dendritic Cells

2000

Contact sensitivity is a T-cell-mediated immune disease that can occur when low-molecular-weight chemicals penetrate the skin. In vivo topical application of chemical sensitizers results in morphological modification of Langerhans cells (LC). Moreover, within 18 h, LC increase their major histocompatibility complex (MHC) class II antigens expression and migrate to lymph nodes where they present the sensitizer to T lymphocytes. We wanted to determine if such an effect could also be observed in vitro. However, because of the high genetic diversity encountered in humans, assays were performed with dendritic cells (DC) obtained from a Balb/c mouse strain. The capacity of a strong sensitizer, DN…

Health Toxicology and MutagenesisGenes MHC Class IIBone Marrow CellsSodium ChlorideBiologyAnimal Testing AlternativesToxicologyMajor histocompatibility complexCell LineImmunophenotypingOxazoloneMicechemistry.chemical_compoundImmune systemAntigens CDIn vivoCell AdhesionmedicineAnimalsDimethyl SulfoxideBenzothiazolesCells CulturedSensitizationMice Inbred BALB CMHC class IIHistocompatibility Antigens Class IIOxazoloneSodium Dodecyl SulfateDendritic CellsDendritic cellMolecular biologyIn vitroThiazolesmedicine.anatomical_structureGene Expression RegulationchemistryAntigens SurfaceDermatitis Allergic ContactImmunologyIrritantsbiology.proteinDinitrofluorobenzeneFemaleHaptensIn Vitro & Molecular Toxicology
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Epigenetic and in vivo comparison of diverse MSC sources reveals an endochondral signature for human hematopoietic niche formation

2015

In the last decade there has been a rapid expansion in clinical trials using mesenchymal stromal cells (MSCs) from a variety of tissues. However, despite similarities in morphology, immunophenotype, and differentiation behavior in vitro, MSCs sourced from distinct tissues do not necessarily have equivalent biological properties. We performed a genome-wide methylation, transcription, and in vivo evaluation of MSCs from human bone marrow (BM), white adipose tissue, umbilical cord, and skin cultured in humanized media. Surprisingly, only BM-derived MSCs spontaneously formed a BM cavity through a vascularized cartilage intermediate in vivo that was progressively replaced by hematopoietic tissue…

Hematopoiesis and Stem CellsCellular differentiationBlotting WesternImmunologyCD34Bone Marrow CellsBiologyBiochemistryEpigenesis GeneticOsteogenesismedicineHumansCell LineageStem Cell NichefungiMesenchymal stem cellHematopoietic Tissuefood and beveragesCell DifferentiationMesenchymal Stem CellsCell BiologyHematologyAnatomyFlow CytometryHematopoietic Stem CellsCell biologyTransplantationmedicine.anatomical_structureBone marrowStem cellChondrogenesisHoming (hematopoietic)Blood
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Direct Toll-Like Receptor-Mediated Stimulation of Hematopoietic Stem and Progenitor Cells Occurs In Vivo and Promotes Differentiation Toward Macropha…

2012

Abstract As Toll-like receptors (TLRs) are expressed by hematopoietic stem and progenitor cells (HSPCs), they may play a role in hematopoiesis in response to pathogens during infection. We show here that TLR2, TLR4, and TLR9 agonists (tripalmitoyl-S-glyceryl-L-Cys-Ser-(Lys)4 [Pam3CSK4], lipopolysaccharide [LPS], and CpG oligodeoxynucleotide [ODN]) induce the in vitro differentiation of purified murine lineage negative cells (Lin−) as well as HSPCs (identified as Lin− c-Kit+ Sca-1+ IL-7Rα− [LKS] cells) toward macrophages (Mph), through a myeloid differentiation factor 88 (MyD88)-dependent pathway. In order to investigate the possible direct interaction of soluble microorganism-associated mol…

Hematopoietic stem and progenitor cellsBiologyCell LineMicemedicineAnimalsProgenitor cellToll-like receptorInnate immune systemMacrophagesToll-Like ReceptorsTLR9Cell DifferentiationCell BiologyFlow CytometryHematopoietic Stem CellsMyD88Molecular biologyToll-Like Receptor 2Toll-like receptorsMice Inbred C57BLToll-Like Receptor 4TLR2Haematopoiesismedicine.anatomical_structureMyeloid Differentiation Factor 88TLR4Molecular MedicineBone marrowDevelopmental BiologySignal Transduction
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