Search results for "keratinocyte"

showing 10 items of 121 documents

The Ras/Raf-1/MEK1/ERK Signaling Pathway Coupled to Integrin Expression Mediates Cholinergic Regulation of Keratinocyte Directional Migration

2005

The physiologic mechanisms that determine directionality of lateral migration are a subject of intense research. Galvanotropism in a direct current (DC) electric field represents a natural model of cell re-orientation toward the direction of future migration. Keratinocyte migration is regulated through both the nicotinic and muscarinic classes of acetylcholine (ACh) receptors. We sought to identify the signaling pathway mediating the cholinergic regulation of chemotaxis and galvanotropism. The pharmacologic and molecular modifiers of the Ras/Raf-1/MEK1/ERK signaling pathway altered both chemotaxis toward choline and galvanotropism toward the cathode in a similar way, indicating that the sam…

KeratinocytesMAPK/ERK pathwayIntegrinsalpha7 Nicotinic Acetylcholine ReceptorMAP Kinase Signaling SystemIntegrinMAP Kinase Kinase 1Receptors NicotinicBiologyTransfectionBiochemistryMuscarinic acetylcholine receptormedicineHumansRNA Small InterferingKeratinocyte migrationExtracellular Signal-Regulated MAP KinasesMolecular BiologyCells CulturedChemotaxisReceptor Muscarinic M1ChemotaxisCell BiologyAcetylcholineUp-RegulationCell biologyElectrophysiologyras Proteinsbiology.proteinraf KinasesLamellipodiumSignal transductionAcetylcholineSignal Transductionmedicine.drugJournal of Biological Chemistry
researchProduct

Imiquimod-Induced Psoriasis in Mice Depends on the IL-17 Signaling of Keratinocytes

2018

The pathology of psoriasis strongly depends on IL-17A. Monoclonal antibodies blocking either the cytokine or its receptor are among the most efficient treatments for psoriatic patients. Keratinocytes can be activated upon exposure to IL-17A and tumor necrosis factor-α and secrete secondary cytokines and chemokines in the inflamed skin. In psoriasis and its imiquimod-induced mouse model, a strong skin infiltration of neutrophils and inflammatory monocytes can be observed. However, to date, it is not clear how exactly those cellular populations are attracted to the skin and how they contribute to the pathogenesis of the disease. To define the crucial cell type responding to IL-17 and initiati…

KeratinocytesMale0301 basic medicineCell typeChemokinemedicine.medical_treatmentImiquimodDermatologyReal-Time Polymerase Chain ReactionBiochemistryMiceRandom Allocation03 medical and health sciences0302 clinical medicineAdjuvants ImmunologicPsoriasismedicineAnimalsPsoriasisMolecular BiologyCells CulturedImiquimodbiologyTumor Necrosis Factor-alphabusiness.industryBiopsy NeedleInterleukin-17Cell BiologyFlow Cytometrymedicine.diseaseImmunohistochemistryMice Inbred C57BLDisease Models Animal030104 developmental biologyCytokinemedicine.anatomical_structure030220 oncology & carcinogenesisImmunologybiology.proteinCytokinesFemaleTumor necrosis factor alphaInterleukin 17KeratinocytebusinessSignal Transductionmedicine.drugJournal of Investigative Dermatology
researchProduct

Epigenetic control of IL-23 expression in keratinocytes is important for chronic skin inflammation

2018

The chronic skin inflammation psoriasis is crucially dependent on the IL-23/IL-17 cytokine axis. Although IL-23 is expressed by psoriatic keratinocytes and immune cells, only the immune cell-derived IL-23 is believed to be disease relevant. Here we use a genetic mouse model to show that keratinocyte-produced IL-23 is sufficient to cause a chronic skin inflammation with an IL-17 profile. Furthermore, we reveal a cell-autonomous nuclear function for the actin polymerizing molecule N-WASP, which controls IL-23 expression in keratinocytes by regulating the degradation of the histone methyltransferases G9a and GLP, and H3K9 dimethylation of the IL-23 promoter. This mechanism mediates the inducti…

KeratinocytesMale0301 basic medicinemedicine.medical_treatmentWiskott-Aldrich Syndrome Protein NeuronalGeneral Physics and AstronomyEpigenesis GeneticHistonesMice0302 clinical medicineGenes ReporterInterleukin 23Promoter Regions Geneticlcsh:ScienceSkinMice KnockoutMultidisciplinaryInterleukin-17QMiddle AgedCytokine030220 oncology & carcinogenesisHistone methyltransferaseTumor necrosis factor alphaSignal transductionmedicine.symptomSignal TransductionAdultScienceGreen Fluorescent ProteinsPrimary Cell CultureInflammationBiologyArticleGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesImmune systemPsoriasismedicineAnimalsHumansPsoriasisInflammationHistone-Lysine N-MethyltransferaseGeneral Chemistrybiochemical phenomena metabolism and nutritionmedicine.diseaseDisease Models AnimalHEK293 Cells030104 developmental biologyInterleukin-23 Subunit p19Cancer researchlcsh:QNature Communications
researchProduct

In contrast to their murine counterparts, normal human keratinocytes and human epidermoid cell lines A431 and HaCaT fail to express IL-10 mRNA and pr…

1997

Abstract In mice, keratinocyte-derived IL-10 is up-regulated by ultraviolet-B (UVB) radiation and plays a major role in UVB-induced immunosuppression. The present study was designed to examine whether a comparable phenomenon can be detected in man. Freshly isolated or cultured normal human keratinocytes (NHK) and keratinocyte cell lines A431 and HaCaT were stimulated with graded doses of UVB (up to 200 J/m2) or with a variety of other stimuli. RNA was extracted at various time points post-stimulation and analysed by reverse transcriptase-polymerase chain reaction (RT-PCR) using four different IL-10-specific primer pairs and RNA from monocytes or T cells as positive controls. We failed to de…

KeratinocytesMaleCell typeUltraviolet Raysmedicine.medical_treatmentImmunologyBiologyMelanocyteEpitheliumMicemedicineTumor Cells CulturedImmunology and AllergyAnimalsHumansRNA MessengerMessenger RNAEpidermis (botany)integumentary systemOriginal ArticlesInterleukin-10HaCaTCytokinemedicine.anatomical_structureCell cultureImmunologyMelanocytesKeratinocyteClinical and experimental immunology
researchProduct

Effect of boldine, secoboldine, and boldine methine on angiotensin II-induced neutrophil recruitment in vivo.

2005

AbstractAngiotensin-II (Ang-II) has inflammatory activity and is involved in different diseases associated with the cardiovascular system. This study has evaluated the effect of boldine (B), and two phenanthrene alkaloids semisynthesized by us, secoboldine (SB) and boldine methine (BM), on Ang-II-induced neutrophil recruitment. Intraperitoneal administration of 1 nM Ang-II induced significant neutrophil accumulation, which was maximal at 4–8 h. BM inhibited neutrophil infiltration into the peritoneal cavity at 4 h and 8 h by 73% and 77%, respectively, SB at 8 h by 55%, and B had no effect on this response. Although BM inhibited the release of cytokine-inducible neutrophil chemoattractant/ke…

KeratinocytesMaleChemokineAporphinesEndotheliumNeutrophilsImmunologyChemokine CXCL2InflammationPharmacologyRats Sprague-Dawleychemistry.chemical_compoundIn vivomedicineImmunology and AllergyBoldineAnimalsHumansInfusions ParenteralPlatelet Activating FactorReceptorchemistry.chemical_classificationReactive oxygen speciesbiologyMolecular StructureAngiotensin IIMonokinesInterleukin-8Endothelial CellsCell BiologyPhenanthrenesAngiotensin IIRatsP-Selectinmedicine.anatomical_structureBiochemistrychemistrybiology.proteinIntercellular Signaling Peptides and Proteinsmedicine.symptomChemokinesReactive Oxygen SpeciesChemokines CXCJournal of leukocyte biology
researchProduct

Use of a collagen/elastin-membrane for the tissue engineering of dermis.

1999

In an experimental model in rats, xenogeneic membranes consisting of processed native collagen and elastin were grafted to serve as a template for the formation of a neo-dermis, while in vitro-cultured autogeneic keratinocytes were applied on top of this to restore an epidermis. The process of tissue reconstruction and the digestion of the grafted membrane components were analysed by histological and immunohistochemical methods as well as electron microscopy. Approximately 3 weeks post grafting the membranes were completely vascularised and colonized by different types of cells. After 6 weeks, the collagenous fibres of the graft were mostly replaced by newly formed collagenous texture, wher…

KeratinocytesMaleDermatologic Surgical ProceduresNeovascularization PhysiologicHuman skinCritical Care and Intensive Care MedicineDermisTissue engineeringMedicineAnimalsCells CulturedSkinUltrasonographyBasement membraneSkin Artificialbiologybusiness.industryRats Inbred StrainsGeneral MedicineAnatomyEpitheliumElastinRatsMicroscopy Electronmedicine.anatomical_structureMembraneEmergency Medicinebiology.proteinBiophysicsMicroscopy Electron ScanningSurgeryEpidermisCollagenbusinessElastinBurns : journal of the International Society for Burn Injuries
researchProduct

Granulocyte–Macrophage Colony-Stimulating Factor Is Essential for Normal Wound Healing

2006

Granulocyte-macrophage colony-stimulating factor (GM-CSF) is a multipotent growth factor, which plays an important role during the process of wound healing. In clinical settings it has occasionally been employed in the treatment of cutaneous wounds of diverse etiologies. In a previous study, we have shown the positive influence of GM-CSF on full thickness excisional wounds in transgenic mice overexpressing GM-CSF in the basal layer of the epidermis. Direct GM-CSF action as well as indirect processes through the induction of secondary cytokines were proposed to contribute towards the beneficial effects. In this study, we analyzed the process of wound healing in transgenic mice overexpressing…

KeratinocytesMaleGenetically modified mousePathologymedicine.medical_specialtyPulmonary Fibrosismedicine.medical_treatmentNeovascularization PhysiologicMice TransgenicDermatologyNeovascularizationMiceBasal (phylogenetics)FibrosismedicineAnimalsMolecular BiologyCell ProliferationWound HealingEpidermis (botany)business.industryGrowth factorGranulocyte-Macrophage Colony-Stimulating FactorCell BiologyGeneral Medicinemedicine.diseaseGranulocyte macrophage colony-stimulating factorGranulation TissueCancer researchFemalemedicine.symptomWound healingbusinessBiotechnologymedicine.drugJournal of Investigative Dermatology Symposium Proceedings
researchProduct

Oxidative DNA damage induced by visible light in mammalian cells: extent, inhibition by antioxidants and genotoxic effects

1998

The extent of the indirect DNA damage generated in mammalian cells by visible light because of the presence of endogenous photosensitizers was studied by means of repair endonucleases. In immortalized human keratinocytes (HaCaT cells) exposed to low doses of natural sunlight, the yield of oxidative DNA base modifications sensitive to the repair endonuclease formamidopyrimidine-DNA glycosylase (Fpg protein) generated by this indirect mechanism was 10% of that of pyrimidine dimers (generated by direct DNA excitation). A similar yield of Fpg-sensitive modifications, which include 8-hydroxyguanine, was observed in primary keratinocytes. The relative yield of oxidative base modifications decreas…

KeratinocytesMalePorphyrinsLightDNA damageRiboflavinPyrimidine dimerAscorbic AcidBiologyToxicologyIndirect DNA damageAntioxidantsMiceCricetinaeGeneticsAnimalsHumansN-Glycosyl HydrolasesMolecular BiologyCells CulturedMutagenesisInfant NewbornInfantEndonucleasesAscorbic acidHaCaTDNA-Formamidopyrimidine GlycosylaseBiochemistryMutagenesisDNA glycosylaseChild PreschoolBiophysicsL1210 cellsOxidation-ReductionDNA DamageMutation Research/DNA Repair
researchProduct

NF-κB and STAT3 Inhibition as a Therapeutic Strategy in Psoriasis: In Vitro and In Vivo Effects of BTH

2013

Benzo[b]thiophen-2-yl-3-bromo-5-hydroxy-5H-furan-2-one (BTH) is a simple and interesting synthetic derivative of petrosaspongiolide M, a natural compound isolated from a sea sponge with demonstrated potent anti-inflammatory activity through inhibition of the NF-κB signaling pathway. In the present study, we report the in vitro and in vivo pharmacological effect of BTH on some parameters related to the innate and adaptive response in the pathogenesis of psoriasis. BTH inhibited the release of some of the key psoriatic cytokines such as tumor necrosis factor α, IL-8, IL-6, and CCL27 through the downregulation of NF-κB in normal human keratinocytes. Moreover, it impaired signal transducers and…

KeratinocytesMaleSTAT3 Transcription FactorForeskinPrimary Cell CultureDermatitisInflammationDermatologyPharmacologyBiochemistryMicechemistry.chemical_compoundIn vivoPsoriasisThiadiazolesmedicineAnimalsHumansPsoriasisSTAT3Molecular BiologyCell ProliferationMice Inbred BALB CbiologyNF-kappa BNF-κBCell Biologymedicine.diseaseDisease Models Animalmedicine.anatomical_structurechemistrybiology.proteinCytokinesFemaleCCL27Signal transductionmedicine.symptomKeratinocyteJournal of Investigative Dermatology
researchProduct

Unsaturated Fatty Acids Drive Disintegrin and Metalloproteinase (ADAM)-dependent Cell Adhesion, Proliferation, and Migration by Modulating Membrane F…

2011

The disintegrin-metalloproteinases ADAM10 and ADAM17 mediate the release of several cell signaling molecules and cell adhesion molecules such as vascular endothelial cadherin or L-selectin affecting endothelial permeability and leukocyte transmigration. Dysregulation of ADAM activity may contribute to the pathogenesis of vascular diseases, but the mechanisms underlying the control of ADAM functions are still incompletely understood. Atherosclerosis is characterized by lipid plaque formation and local accumulation of unsaturated free fatty acids (FFA). Here, we show that unsaturated FFA increase ADAM-mediated substrate cleavage. We demonstrate that these alterations are not due to genuine ch…

KeratinocytesMembrane FluidityADAM10Lipid BilayersVascular permeabilityBiologyADAM17 ProteinBiochemistryCapillary PermeabilityADAM10 ProteinCell MovementMembrane fluidityCell AdhesionAnimalsHumansCell adhesionMolecular BiologyCell ProliferationCell adhesion moleculeCell growthFluorescence recovery after photobleachingEndothelial CellsMembrane ProteinsCell BiologyAtherosclerosisADAM ProteinsCell biologyLipoproteins LDLADAM ProteinsHEK293 CellsFatty Acids UnsaturatedCholesterol EstersRabbitsAmyloid Precursor Protein SecretasesGranulocytes
researchProduct