Search results for "Downregulation"

showing 10 items of 460 documents

The Neuronal Nitric Oxide Synthase Is Upregulated in Mouse Skin Repair and in Response to Epidermal Growth Factor in Human HaCaT Keratinocytes

2004

Expression of nNOS mRNA was found in normal human and mouse skin tissue. Upon wounding, we observed a rapid downregulation of nNOS mRNA and protein in wounds of mice; however, when repair continued, nNOS mRNA was strongly upregulated and nNOS protein expression peaked at late stages of healing. Immunohistochemistry revealed wound keratinocytes as the cellular source of nNOS. In line with the in vivo situation, we found a basal expression of nNOS in the human keratinocyte cell line HaCaT. A marked stimulation of nNOS expression in the cells was achieved with epidermal growth factor receptor (EGFR) ligands such as epidermal growth factor (EGF), heparin-binding EGF, transforming growth factor-…

Keratinocytesinorganic chemicalsReceptor ErbB-3Receptor ErbB-2medicine.medical_treatmentwound healingNitric Oxide Synthase Type IDermatologyBiochemistryGene Expression Regulation EnzymologicCell LineMiceDownregulation and upregulationnitric oxideEpidermal growth factormedicineAnimalsHumansRNA MessengerEpidermal growth factor receptorMolecular BiologySkinMice Inbred BALB CEpidermal Growth Factorintegumentary systembiologyGrowth factorgrowth factorCell BiologyUp-RegulationCell biologyErbB Receptorsbody regionsNitric oxide synthaseHaCaTmedicine.anatomical_structurenervous systemImmunologycardiovascular systembiology.proteinNeuregulinNitric Oxide SynthaseKeratinocyteSignal TransductionJournal of Investigative Dermatology
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Avarol inhibits TNF-a generation and NF-kB activation in human cells and in animal models

2007

Avarol is a marine sesquiterpenoid hydroquinone with interesting pharmacological properties including anti-inflammatory and antipsoriatic effects. In the present study we evaluated the pharmacological effect of avarol on some inflammatory parameters related to the pathogenesis of psoriasis. Avarol inhibited tumor necrosis factor-alpha (TNF-alpha) generation in stimulated human monocytes (IC(50) 1 microM) and TNF-alpha-induced activation of nuclear factor-kappaB (NF-kappaB)-DNA binding in keratinocytes. In the mouse air pouch model, administration of avarol produced a dose-dependent reduction of TNF-alpha generation (ED(50) 9.2 nmol/pouch) as well as of interleukin (IL)-1beta, prostaglandin …

Keratinocytesmedicine.medical_specialtymedicine.medical_treatmentAnti-Inflammatory AgentsAntineoplastic AgentsBiologyPharmacologyMonocytesGeneral Biochemistry Genetics and Molecular BiologyCell LineMicechemistry.chemical_compoundDownregulation and upregulationIn vivoInternal medicinemedicineAnimalsHumansPsoriasisGeneral Pharmacology Toxicology and PharmaceuticsPeroxidaseInflammationHyperplasiaDose-Response Relationship DrugTumor Necrosis Factor-alphaNF-kappa B p50 SubunitInterleukinNF-κBGeneral MedicineDisease Models AnimalEndocrinologymedicine.anatomical_structureEicosanoidchemistryTetradecanoylphorbol AcetateFemaleTumor necrosis factor alphaEpidermisInflammation MediatorsKeratinocyteSesquiterpenesProstaglandin E
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Resistance of keratinocytes to TGFbeta-mediated growth restriction and apoptosis induction accelerates re-epithelialization in skin wounds.

2002

The pleiotropic growth factor TGFβ plays an important role in regulating responses to skin injury. TGFβ targets many different cell types and is involved in all aspects of wound healing entailing inflammation,re-epithelialization, matrix formation and remodeling. To elucidate the role of TGFβ signal transduction in keratinocytes during cutaneous wound healing, we have used transgenic mice expressing a dominant negative type II TGFβ receptor exclusively in keratinocytes. We could demonstrate that this loss of TGFβ signaling in keratinocytes led to an accelerated re-epithelialization of full thickness excisional wounds accompanied by an increased proliferation in keratinocytes at the wound ed…

Keratinocytesmedicine.medical_treatmentEGR1InflammationApoptosisMice TransgenicBiologyImmediate early proteinCell LineImmediate-Early ProteinsMiceDownregulation and upregulationTransforming Growth Factor betamedicineAnimalsTranscription factorEarly Growth Response Protein 1Wound Healingintegumentary systemGrowth factorGene Expression ProfilingCell BiologyCell biologyDNA-Binding ProteinsEpidermal CellsImmunologymedicine.symptomSignal transductionEpidermisWound healingCell DivisionTranscription FactorsJournal of cell science
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Downregulation of KLF8 expression by shRNA induces inhibition of cell proliferation in CAL27 human oral cancer cells

2013

Objectives: KLF8 is a member of KLF transcription factors which play an important tolr in oncogenesis. It is barely expressed in normal human epithelial cells but highly overexpressed in several types of human cancer cell lines. In the present study, we investigate the role of KLF8 in oral cancer and the effects of KLF8 knockdown via lentivirus mediated siRNA infection in human adenosquamos carcinoma CAL 27 cells. Study Design: �e developed a vector-based siRNA expression system that can induce RNAi in CAL 27 oral canDesign: �e developed a vector-based siRNA expression system that can induce RNAi in CAL 27 oral canesign: �e developed a vector-based siRNA expression system that can induce RN…

Kruppel-Like Transcription FactorsDown-RegulationOdontologíaBiologymedicine.disease_causeSmall hairpin RNACarcinoma AdenosquamousDownregulation and upregulationmedicineTumor Cells CulturedGene silencingHumansRNA Small InterferingGeneral DentistryCell ProliferationGene knockdownOral Medicine and PathologyTransfection:CIENCIAS MÉDICAS [UNESCO]Ciencias de la saludRepressor Proteinsstomatognathic diseasesOtorhinolaryngologyCell cultureUNESCO::CIENCIAS MÉDICASCancer cellCancer researchLentivirus InfectionsSurgeryResearch-ArticleMouth NeoplasmsCarcinogenesisMedicina Oral, Patología Oral y Cirugía Bucal
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Bisphenol-A impairs insulin action and up-regulates inflammatory pathways in human subcutaneous adipocytes and 3T3-L1 cells.

2013

Current evidence indicates that chemical pollutants may interfere with the homeostatic control of nutrient metabolism, thereby contributing to the increased prevalence of metabolic disorders. Bisphenol-A (BPA) is a lipophilic compound contained in plastic which is considered a candidate for impairing energy and glucose metabolism. We have investigated the impact of low doses of BPA on adipocyte metabolic functions. Human adipocytes derived from subcutaneous adipose tissue and differentiated 3T3-L1 cells were incubated with BPA, in order to evaluate the effect on glucose utilization, insulin sensitivity and cytokine secretion. Treatment with 1 nM BPA significantly inhibited insulin-stimulate…

Leptinmedicine.medical_treatmentAdipose tissuechemistry.chemical_compoundMice0302 clinical medicineAdipocyteAdipocytesInsulinPhosphorylation0303 health sciencesMultidisciplinaryPERSISTENT ORGANIC POLLUTANTS BODY-MASS INDEX METABOLIC SYNDROME ENVIRONMENTAL CONTAMINANTS CARDIOVASCULAR-DISEASE ENDOCRINE DISRUPTORS SERUM CONCENTRATIONS WIDESPREAD EXPOSURE PERINATAL EXPOSURE DIABETES-MELLITUSbiologyQRNF-kappa BCell Differentiation3. Good healthUp-RegulationAdipogenesisMedicinehormones hormone substitutes and hormone antagonistsResearch ArticleSignal TransductionSTAT3 Transcription Factormedicine.medical_specialtyendocrine systemScienceSubcutaneous FatDown-Regulation030209 endocrinology & metabolism03 medical and health sciencesDownregulation and upregulationPhenolsInternal medicine3T3-L1 CellsmedicineAnimalsHumansRNA MessengerBenzhydryl Compounds030304 developmental biologyInflammationurogenital systemInsulinJNK Mitogen-Activated Protein KinasesReceptor InsulinInsulin receptorEndocrinologyGlucosechemistry13. Climate actionbiology.proteinCytokine secretionGLUT4PloS one
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Severe metabolic alterations in liver cancer lead to ERK pathway activation and drug resistance

2020

Background: The extracellular signal-regulated kinase (ERK) pathway regulates cell growth, and is hyper-activated and associated with drug resistance in hepatocellular carcinoma (HCC). Metabolic pathways are profoundly dysregulated in HCC. Whether an altered metabolic state is linked to activated ERK pathway and drug response in HCC is unaddressed. Methods: We deprived HCC cells of glutamine to induce metabolic alterations and performed various assays, including metabolomics (with 13C-glucose isotope tracing), microarray analysis, and cell proliferation assays. Glutamine-deprived cells were also treated with kinase inhibitors (e.g. Sorafenib, Erlotinib, U0126 amongst other MEK inhibitors). …

Life sciences; biology0301 basic medicineSorafenibMAPK/ERK pathwayCarcinoma HepatocellularResearch paperMAP Kinase Signaling SystemGlutamineProliferationlcsh:MedicineAntineoplastic AgentsGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciences0302 clinical medicineDownregulation and upregulationddc:570medicineSerineHumansHCCProtein Kinase InhibitorsCell Proliferationlcsh:R5-920Cell growthChemistryKinaseMicroarray analysis techniquesLiver Neoplasmslcsh:RGeneral MedicineHep G2 Cellsdigestive system diseasesMetabolic pathway030104 developmental biologyAnaerobic glycolysisDrug Resistance NeoplasmKinase inhibitors030220 oncology & carcinogenesisCancer researchMetabolomeMetabolic stateAerobic glycolysisTranscriptomelcsh:Medicine (General)medicine.drugEBioMedicine
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Evolutionary and transcriptional analyses of a pentraxin-like component family involved in the LPS inflammatory response of Ciona robusta

2020

Pentraxins (PTXs) are a superfamily of conserved proteins which are components of the humoral arm of innate immunity. They are considered to be functional ancestors of antibodies and are classified into short and long types. In this study, we show that a pentraxin-like component (Ptx-like) with a C-terminal PTX domain, highly homologous to the short PTX of H. sapiens CRP, and a long N-terminal domain typical of long PTXs, is involved in the inflammatory response of Ciona robusta under LPS exposure in vivo. Analyses of protein domains as well as 3D modelling and phylogenetic tree supported the close relationship of Ptx-like with mammalian CRP, suggesting that C. robusta Ptx-like shares a com…

Lipopolysaccharides3D model0301 basic medicineLPSTranscription GeneticProtein domainSettore BIO/05 - ZoologiaChordateSettore BIO/08 - AntropologiaAquatic ScienceEvolution Molecular03 medical and health sciencesDownregulation and upregulationIn vivoAnimalsEnvironmental ChemistryCiona robustaPTXsInflammationInnate immune systemPentraxinsbiologyPhylogenetic tree04 agricultural and veterinary sciencesGeneral Medicinebiology.organism_classificationImmunity InnateCiona intestinalisCell biologyC-Reactive Protein030104 developmental biologyMultigene Family040102 fisheriesbiology.protein0401 agriculture forestry and fisheriesAntibodyFish & Shellfish Immunology
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Resveratrol decreases the levels of miR-155 by upregulating miR-663, a microRNA targeting JunB and JunD.

2010

An inflammatory component is present in the microenvironment of most neoplastic tissues, including those not causally related to an obvious inflammatory process. Several microRNAs, and especially miR-155, play an essential role in both the innate and adaptative immune response. Resveratrol (trans-3,4#,5-trihydroxystilbene) is a natural antioxidant with anti-inflammatory properties that is currently at the stage of preclinical studies for human cancer prevention. Here, we establish that, in human THP-1 monocytic cells as well as in human blood monocytes, resveratrol upregulates miR- 663, a microRNA potentially targeting multiple genes implicated in the immune response. In THP-1 cells, miR-66…

LipopolysaccharidesCancer ResearchJUNBProto-Oncogene Proteins c-junBlotting WesternResveratrolBiologyMonocytesmiR-15503 medical and health scienceschemistry.chemical_compound0302 clinical medicineImmune systemDownregulation and upregulationRNA interferencemicroRNAStilbenesBiomarkers TumorHumans[SDV.BBM]Life Sciences [q-bio]/Biochemistry Molecular BiologyRNA MessengerLuciferases[ SDV.BBM ] Life Sciences [q-bio]/Biochemistry Molecular BiologyCells Cultured030304 developmental biologyOligonucleotide Array Sequence AnalysisCancer Biology0303 health sciencesInnate immune systemmicroRNAReverse Transcriptase Polymerase Chain ReactionGene Expression ProfilingmicroRNA; ResveratrolGeneral MedicineAntineoplastic Agents Phytogenic3. Good healthUp-RegulationTranscription Factor AP-1MicroRNAschemistryGene Expression RegulationResveratrol030220 oncology & carcinogenesisCancer research
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Reduced expression of TLR4 is associated with the metastatic status of human colorectal cancer.

2007

Signaling mediating colorectal cancer (CRC) progression is incompletely understood. Previously, we identified lipopolysaccharide (LPS), an endotoxin of ubiquitously existing colonic bacteria, as a pivotal stimulus increasing the metastatic potential of human CRC. Since the ubiquitous colonic bacteria release large amounts of LPS this observation could be of enormous relevance for the progression of CRC. In this study we present data contributing to the elucidation of its mode of action. Since both receptors CD14 and TLR4 act as LPS mediators, we determined their expression in various CRC cell lines and in 115 non-metastatic, lymphogenous-metastatic and haematogenous-metastatic CRC specimens…

LipopolysaccharidesColorectal cancerCellLipopolysaccharide ReceptorsBiologyDownregulation and upregulationCell Line TumorGeneticsmedicineHumansNeoplasm MetastasisReceptorFluorescent Antibody Technique IndirectNeoplasm StagingRetrospective StudiesOncogeneCarcinomaGeneral MedicineCell cyclemedicine.diseaseMolecular medicineImmunohistochemistrydigestive system diseasesGene Expression Regulation NeoplasticToll-Like Receptor 4medicine.anatomical_structureLymphatic MetastasisImmunologyTLR4Cancer researchlipids (amino acids peptides and proteins)Caco-2 CellsColorectal NeoplasmsInternational journal of molecular medicine
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Phosphate Groups in the Lipid A Moiety Determine the Effects of LPS on Hepatic Stellate Cells: A Role for LPS-Dephosphorylating Activity in Liver Fib…

2020

Alkaline phosphatase (AP) activity is highly upregulated in plasma during liver diseases. Previously, we demonstrated that AP is able to detoxify lipopolysaccharide (LPS) by dephosphorylating its lipid A moiety. Because a role of gut-derived LPS in liver fibrogenesis has become evident, we now examined the relevance of phosphate groups in the lipid A moiety in this process. The effects of mono-phosphoryl and di-phosphoryl lipid A (MPLA and DPLA, respectively) were studied in vitro and LPS-dephosphorylating activity was studied in normal and fibrotic mouse and human livers. The effects of intestinal AP were studied in mice with CCL4-induced liver fibrosis. DPLA strongly stimulated fibrogenic…

LipopolysaccharidesLiver CirrhosisMale0301 basic medicinemedicine.medical_specialtyLipopolysaccharideNitric OxideArticleLipid AMice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineDownregulation and upregulationInternal medicinemedicineAnimalsMacrophagePhosphorylationlipid Alcsh:QH301-705.5liver fibrosisMice Inbred BALB CInterleukin-6MacrophageslipopolysaccharideBiological activityGeneral MedicineIn vitroRatsUp-RegulationRAW 264.7 Cells030104 developmental biologyEndocrinologyLiverchemistrylcsh:Biology (General)Hepatic stellate cellAlkaline phosphatase030211 gastroenterology & hepatologylipids (amino acids peptides and proteins)hepatic stellate cellsalkaline phosphatase
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