Search results for "InAs"

showing 10 items of 4155 documents

Activation of microglia synergistically enhances neurodegeneration caused by MPP+ in human SH-SY5Y cells

2019

While MPP+ may not directly activate microglia, the initial neuronal damage inflicted by the toxin may trigger microglia, possibly leading to synergistic pro-apoptotic interaction between neuro-inflammation and toxin-induced neurotoxicity, which may further aggravate neurodegeneration. However, what molecular targets are synergistically up or downregulated during this interaction is not well understood. Here, we addressed this by co-culturing fully differentiated human SH-SY5Y cells treated with parkinsonian toxin 1-Methyl-4-phenylpyridinium (MPP+), with endotoxin-activated microglial cell line EOC 20 to determine how this interaction affects pro-apoptotic (p38, JNK, and bax:bcl2 ratios) an…

0301 basic medicinePharmacologySH-SY5YMicrogliaChemistryp38 mitogen-activated protein kinasesNeurodegenerationNeurotoxicityInflammationmedicine.diseaseCell biology03 medical and health sciences030104 developmental biology0302 clinical medicinemedicine.anatomical_structureApoptosismedicineViability assaymedicine.symptom030217 neurology & neurosurgeryEuropean Journal of Pharmacology
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Chemoresistance and chemosensitization in cholangiocarcinoma

2017

One of the main difficulties in the management of patients with advanced cholangiocarcinoma (CCA) is their poor response to available chemotherapy. This is the result of powerful mechanisms of chemoresistance (MOC) of quite diverse nature that usually act synergistically. The problem is often worsened by altered MOC gene expression in response to pharmacological treatment. Since CCA includes a heterogeneous group of cancers their genetic signature coding for MOC genes is also diverse; however, several shared traits have been defined. Some of these characteristics are shared with other types of liver cancer, namely hepatocellular carcinoma and hepatoblastoma. An important goal in modern onco…

0301 basic medicinePharmacologybile ductschemotherapydrug delivery systems0302 clinical medicineChemosensitizationantineoplastic agentsmolecular biologyReceptorhumansreceptor protein-tyrosine kinasesmedia_commonapoptosisgene expression regulationbile duct neoplasmsDrug Resistance Multipletargeted therapiesGene Expression Regulation Neoplasticmultiplebiliary cancer; chemotherapy; liver cancer; multidrug resistance; targeted therapies; antineoplastic agents; apoptosis; bile duct neoplasms; bile ducts; cell survival; cholangiocarcinoma; drug delivery systems; drug resistance multiple; drug resistance; neoplasm; epithelial cells; gene expression regulation neoplastic; genetic therapy; humans; protein kinase inhibitors; receptor protein-tyrosine kinases; signal transduction; treatment outcome; molecular medicine; molecular biology030220 oncology & carcinogenesisHepatocellular carcinomabiliary cancerLiver cancercholangiocarcinomaTyrosine kinasesignal transductionDrugHepatoblastomamedia_common.quotation_subjectcell survivalPharmacological treatmentliver cancer03 medical and health sciencesmultidrug resistancemedicinemolecular medicinedrug resistancebusiness.industrymedicine.diseaseepithelial cellsneoplasticprotein kinase inhibitors030104 developmental biologyDrug Resistance NeoplasmCancer researchtreatment outcomebusinessneoplasmgenetic therapy
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Silencing of C3G increases cardiomyocyte survival inhibition and apoptosis via regulation of p-ERK1/2 and Bax.

2018

Experimental studies have shown that overexpression of Rap guanine nucleotide exchange factor 1 (C3G) plays pro-survival and anti-apoptotic roles through molecule phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2) in cardiomyocytes. However, it is still unclear if silencing of C3G may increase cell survival inhibition and apoptosis in cardiomyocytes, and whether C3G silence induced injuries are reduced by the overexpression of C3G through regulation of p-ERK1/2 and pro-apoptotic molecule Bax. In this study, the rat-derived H9C2 cardiomyocytes were infected with C3G small hairpin RNA interference recombinant lentiviruses, which silenced the endogenous C3G expression in the ca…

0301 basic medicinePhysiologyCell SurvivalEndogenyApoptosisCell LineSmall hairpin RNA03 medical and health sciences0302 clinical medicinePhysiology (medical)ExtracellularmedicineGene silencingAnimalsMyocytes CardiacGene SilencingGuanine Nucleotide-Releasing Factor 2Cell Proliferationbcl-2-Associated X ProteinPharmacologyMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Cell growthChemistryHypoxia (medical)PhosphoproteinsCell biologyRats030104 developmental biologyApoptosis030220 oncology & carcinogenesisPhosphorylationmedicine.symptomClinical and experimental pharmacologyphysiology
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Comparative Proteomics Unveils LRRFIP1 as a New Player in the DAPK1 Interactome of Neurons Exposed to Oxygen and Glucose Deprivation

2020

Altres ajuts: The group has received funding from 'la Caixa Foundation' CI15-00009, from the European Institute of Innovation and Technology (EIT) PoC-2016-SPAIN-04, which receives support from the European Union's Horizon 2020 research and innovation program, and from the 'Fundación para la Innovación y la Prospectiva en Salud en España (FIPSE)' program 3594-18. Death-associated protein kinase 1 (DAPK1) is a pleiotropic hub of a number of networked distributed intracellular processes. Among them, DAPK1 is known to interact with the excitotoxicity driver NMDA receptor (NMDAR), and in sudden pathophysiological conditions of the brain, e.g., stroke, several lines of evidence link DAPK1 with t…

0301 basic medicinePhysiologyClinical BiochemistryExcitotoxicitymedicine.disease_causeProteomicsBiochemistryInteractomeNeuroprotectionArticle03 medical and health sciences0302 clinical medicinemedicineDAPK1Protein kinase AMolecular Biologychemistry.chemical_classificationReactive oxygen specieslcsh:RM1-950OGDROSCell BiologyneuronferroptosisCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. Pharmacologychemistrynervous systemNMDANeuronLRRFIP1MCAO030217 neurology & neurosurgeryIntracellularAntioxidants
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A conditional inducible JAK2V617F transgenic mouse model reveals myeloproliferative disease that is reversible upon switching off transgene expressio…

2019

Aberrant activation of the JAK/STAT pathway is thought to be the critical event in the pathogenesis of the chronic myeloproliferative neoplasms, polycythemia vera, essential thrombocythemia and primary myelofibrosis. The most frequent genetic alteration in these pathologies is the activating JAK2V617F mutation, and expression of the mutant gene in mouse models was shown to cause a phenotype resembling the human diseases. Given the body of genetic evidence, it has come as a sobering finding that JAK inhibitor therapy only modestly suppresses the JAK2V617F allele burden, despite showing clear benefits in terms of reducing splenomegaly and constitutional symptoms in patients. To gain a better …

0301 basic medicinePhysiologyClone (cell biology)Mice0302 clinical medicineAnimal CellsBone MarrowImmune PhysiologyMedicine and Health SciencesBlood and Lymphatic System ProceduresTransgenesBone Marrow TransplantationRegulation of gene expressionMultidisciplinaryQRAnimal ModelsBody FluidsPhenotypesBloodExperimental Organism Systems030220 oncology & carcinogenesisMedicineAnatomyCellular TypesResearch ArticleGenetically modified mousePlateletsTransgeneScienceImmunologyMutation MissenseMice TransgenicMouse ModelsSurgical and Invasive Medical ProceduresBone Marrow CellsBiologyResearch and Analysis Methods03 medical and health sciencesModel OrganismsmedicineGeneticsAnimalsHumansAlleleProgenitor cellMyelofibrosisMolecular Biology TechniquesMolecular BiologyTransplantationMyeloproliferative DisordersBlood CellsEssential thrombocythemiaBiology and Life SciencesCell BiologyJanus Kinase 2medicine.diseaseHematopoietic Stem CellsDisease Models Animal030104 developmental biologyAmino Acid SubstitutionGene Expression RegulationImmune SystemCancer researchAnimal StudiesSpleenCloningPLoS ONE
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Mesenchymal Stem Cells Improve Glycometabolism and Liver Regeneration in the Treatment of Post-hepatectomy Liver Failure

2019

Background The mortality rate of post-hepatectomy liver failure (PHLF) remains very high, and liver transplantation is the only effective treatment regimen for PHLF. Cell transplantation is a potential treatment for liver diseases. Previous studies have proved that mesenchymal stem cells (MSCs) have immunomodulatory functions. In the present study, we found that MSCs promoted glycogen synthesis and liver regeneration in the treatment of PHLF. MSC transplantation also improved the survival rate of rats after 90% partial hepatectomy (PH). In our current study, we aimed to determine the efficacy and mechanism of MSC transplantation in the treatment of PHLF. Methods Mesenchymal stem cells were …

0301 basic medicinePhysiologymedicine.medical_treatmentPharmacologyLiver transplantationlcsh:Physiology03 medical and health scienceshepatectomy0302 clinical medicinePhysiology (medical)medicinecell transplantationliver regenerationOriginal ResearchLiver injurymesenchymal stem cellslcsh:QP1-981biologybusiness.industryMesenchymal stem cellmedicine.diseaseLiver regenerationglycogen synthesisTransplantation030104 developmental biologyAlanine transaminase030220 oncology & carcinogenesisbiology.proteinHepatectomyStem cellbusinessFrontiers in Physiology
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Prognostic use of soluble fms-like tyrosine kinase-1 and placental growth factor in patients with coronary artery disease.

2015

Background: Intention of the study is to assess the cardiovascular mortality of patients with coronary artery disease (CAD) with the biomarkers of angiogenesis PlGF and its endogenous inhibitor sFlt-1. Methods: The cohort included n = 1848 patients with CAD and 282 subjects without CAD. In 85 patients cardiovascular mortality, as combination of fatal myocardial infarction or any cardiac death, during a median follow-up duration of 3.9 years was reported. Results: In Kaplan–Meier curve analysis PlGF in rising thirds was not predictive regarding outcome (p = 0.54), the same was shown for sFlt-1 (p = 0.44). Cox regression for the fully adjusted model provided a hazard ratio (HR) of 0.8 (p = 0…

0301 basic medicinePlacental growth factorMalemedicine.medical_specialtyClinical BiochemistryCoronary Artery DiseaseKaplan-Meier Estimate030204 cardiovascular system & hematologyPregnancy ProteinsCoronary artery disease03 medical and health scienceschemistry.chemical_compound0302 clinical medicineInternal medicineDrug DiscoveryNatriuretic Peptide BrainmedicineHumansMyocardial infarctionPlacenta Growth FactorVascular Endothelial Growth Factor Receptor-1Proportional hazards modelbusiness.industryBiochemistry (medical)Hazard ratioMiddle Agedmedicine.diseasePrognosisPeptide FragmentsVascular endothelial growth factor030104 developmental biologyEndocrinologychemistryCohortCardiologyFemalebusinessSoluble fms-like tyrosine kinase-1Follow-Up StudiesBiomarkers in medicine
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Cytotoxicity ofSalvia miltiorrhizaAgainst Multidrug-Resistant Cancer Cells

2016

Salvia miltiorrhiza Bunge (Lamiaceae) is a well-known Chinese herb that possesses numerous therapeutic activities, including anticancer effects. In this study, the cytotoxicity and the biological mechanisms of S. miltiorrhiza (SM) root extract on diverse resistant and sensitive cancer cell lines were investigated. CEM/ADR5000 cells were 1.68-fold resistant to CCRF-CEM cells, while HCT116 (p53[Formula: see text] and U87.MG[Formula: see text]EGFR cells were hypersensitive (collateral sensitive) compared to their parental cells. SM root extract stimulated ROS generation, cell cycle S phase arrest and apoptosis. The induction of the intrinsic apoptotic pathway was validated by increased cleavag…

0301 basic medicinePoly ADP ribose polymerasep38 mitogen-activated protein kinasesApoptosisSalvia miltiorrhizaCaspase 3PharmacologyBiologySalvia miltiorrhiza03 medical and health sciences0302 clinical medicineCell Line TumorNeoplasmsHumansCytotoxicityCell Cycle CheckpointsGeneral MedicineCell cycleAntineoplastic Agents PhytogenicMolecular biology030104 developmental biologyComplementary and alternative medicineDrug Resistance NeoplasmApoptosisCaspases030220 oncology & carcinogenesisCancer cellReactive Oxygen SpeciesDrugs Chinese HerbalThe American Journal of Chinese Medicine
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The Intracellular Cleavage Product of the NG2 Proteoglycan Modulates Translation and Cell-Cycle Kinetics via Effects on mTORC1/FMRP Signaling

2018

The NG2 proteoglycan is expressed by oligodendrocyte precursor cells (OPCs) and is abundantly expressed by tumors such as melanoma and glioblastoma. Functions of NG2 include an influence on proliferation, migration and neuromodulation. Similar to other type-1 membrane proteins, NG2 undergoes proteolysis, generating a large ectodomain, a C-terminal fragment (CTF) and an intracellular domain (ICD) via sequential action of α- and γ-secretases which is enhanced by neuronal activity. Functional roles of NG2 have so far been shown for the full-length protein, the released ectodomain and CTF, but not for the ICD. In this study, we characterized the role of the NG2 ICD in OPC and Human Embryonic Ki…

0301 basic medicinePopulationP70-S6 Kinase 1mTORC1γ-secretaselcsh:RC321-57103 medical and health sciencesCellular and Molecular NeuroscienceNG2educationlcsh:Neurosciences. Biological psychiatry. NeuropsychiatryPI3K/AKT/mTOR pathwayOriginal Researcheducation.field_of_studyChemistryICDHEK 293 cellsTranslation (biology)S6K1Cell biologystomatognathic diseases030104 developmental biologyEctodomainnervous systemeEF2mTORPhosphorylationFMRPOPCNeuroscienceFrontiers in Cellular Neuroscience
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Dibutyltin(IV) and Tributyltin(IV) Derivatives of meso-Tetra(4 sulfonatophenyl)porphine Inhibit the Growth and the Migration of Human Melanoma Cells.

2019

Melanoma is the most aggressive and deadly form of skin cancer, which is largely due to its propensity to metastasize. Therefore, with the aim to inhibit the growth and the metastatic dissemination of melanoma cells and to provide a novel treatment option, we studied the effects of the melanoma treatment with two organotin(IV) complexes of the meso-tetra(4-sulfonato-phenyl)porphine, namely (Bu2Sn)2TPPS and (Bu3Sn)4TPPS. In particular, we showed that nanomolar concentrations of (Bu2Sn)2TPPS and (Bu3Sn)4TPPS are sufficient to inhibit melanoma cell growth, to increase the expression of the full-length poly (ADP-ribose) polymerase (PARP-1), to induce the cell cycle arrest respectively at G2/M a…

0301 basic medicinePorphyrinsCellAntineoplastic AgentsApoptosisorganotin(IV)migrationArticleBRAF03 medical and health sciences0302 clinical medicineCyclin D1Cell MovementCell Line Tumormelanoma; organotin(IV); cellular growth; BRAF; cell cycle; migrationmedicinemelanomaHumansSTAT3Cell ProliferationDose-Response Relationship DrugMolecular StructurebiologyCell growthChemistryMelanomaCell migrationCell Cycle CheckpointsGeneral Medicinecellular growthCell cyclemedicine.disease030104 developmental biologymedicine.anatomical_structureFocal Adhesion Kinase 1030220 oncology & carcinogenesisbiology.proteinCancer researchcell cycleSkin cancerSignal Transduction
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