Search results for "Sphingosine"

showing 10 items of 24 documents

Comparative analysis of the effects of a sphingosine kinase inhibitor to temozolomide and radiation treatment on glioblastoma cell lines.

2017

ABSTRACT Glioblastoma multiforme (GBM) exhibits high resistance to the standard treatment of temozolomide (TMZ) combined with radiotherapy, due to its remarkable cell heterogeneity. Accordingly, there is a need to target alternative molecules enhancing specific GBM autocrine or paracrine mechanisms and amplifying the effect of standard treatment. Sphingosine 1-phosphate (S1P) is such a lipid target molecule with an important role in cell invasion and proliferation. Sphingosine kinase inhibitors (SKI) prevent S1P formation and induce increased production of reactive oxygen species (ROS), which may potentiate radiation cytotoxicity. We analyzed the effect of SKI singular versus combined treat…

0301 basic medicineCancer ResearchRadiation-Sensitizing AgentsCell SurvivalCellSphingosine kinaseApoptosistemozolomideBiologyRadiation Tolerancesphingosine kinase inhibition03 medical and health scienceschemistry.chemical_compoundCell Line TumorX-raysmedicineHumansGPx1oxidative stressCytotoxicityAutocrine signallingAntineoplastic Agents AlkylatingPharmacologychemistry.chemical_classificationReactive oxygen speciesTemozolomideSphingosineBrain NeoplasmsDrug SynergismChemoradiotherapyMolecular biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)030104 developmental biologymedicine.anatomical_structureOncologychemistryCell cultureradiosensitivityCancer researchMolecular MedicineDrug Screening Assays AntitumorGlioblastomamedicine.drugResearch PaperCancer biologytherapy
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The sphingosine kinase 1 activator, K6PC-5, attenuates Ebola virus infection

2021

Summary Ebola virus (EBOV) is responsible for outbreaks with case fatality rates of up to 90% and for an epidemic in West Africa with more than ten thousand deaths. EBOV glycoprotein (EBOV-GP) is the only viral surface protein and is responsible for viral entry into cells. Here, by employing pseudotyped EBOV-GP viral particles, we uncover a critical role for sphingolipids in inhibiting viral entry. Sphingosine kinase 1 (SphK1) catalyzes the phosphorylation of sphingosine to sphingosine 1-phosphate (S1P). The administration of the SphK1 activator, K6PC-5, or S1P, or the overexpression of SphK1 consistently exhibited striking inhibitory effects in EBOV-GP-driven entry in diverse cell lines. F…

0301 basic medicineScienceviruses02 engineering and technologymedicine.disease_causeArticle03 medical and health scienceschemistry.chemical_compoundViral entryVirologymedicinechemistry.chemical_classificationMultidisciplinaryEbola virusSphingosinebiologyActivator (genetics)QMolecular MicrobiologyCell Biology021001 nanoscience & nanotechnologyVirologySphingolipid030104 developmental biologychemistrySphingosine kinase 1Cell culturebiology.protein0210 nano-technologyGlycoproteiniScience
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Fingolimod as a Treatment in Neurologic Disorders Beyond Multiple Sclerosis

2020

Abstract Fingolimod is an approved treatment for relapsing–remitting multiple sclerosis (MS), and its properties in different pathways have raised interest in therapy research for other neurodegenerative diseases. Fingolimod is an agonist of sphingosine-1-phosphate (S1P) receptors. Its main pharmacologic effect is immunomodulation by lymphocyte homing, thereby reducing the numbers of T and B cells in circulation. Because of the ubiquitous expression of S1P receptors, other effects have also been described. Here, we review preclinical experiments evaluating the effects of treatment with fingolimod in neurodegenerative diseases other than MS, such as Alzheimer’s disease or epilepsy. Fingolimo…

AgonistSphingosine 1 Phosphate Receptor ModulatorsMultiple Sclerosismedicine.drug_classDrug Evaluation PreclinicalDiseaseReview ArticleRM1-950PharmacologyNeuroprotection03 medical and health sciencesEpilepsyMice0302 clinical medicineNeurotrophic factorsAlzheimer DiseasemedicineAnimalsHumansLymphocytes030304 developmental biologyPharmacology0303 health sciencesEpilepsyMicrogliabusiness.industryFingolimod HydrochlorideMultiple sclerosisAnti-Inflammatory Agents Non-Steroidalmedicine.diseaseFingolimod3. Good healthRatsDisease Models Animalmedicine.anatomical_structureNeuroprotective AgentsTherapeutics. PharmacologyNervous System Diseasesbusiness030217 neurology & neurosurgerymedicine.drugDrugs in R&D
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The lipoprotein receptor LRP1 modulates sphingosine-1-phosphate signaling and is essential for vascular development

2014

Low density lipoprotein receptor-related protein 1 (LRP1) is indispensable for embryonic development. Comparing different genetically engineered mouse models, we found that expression of Lrp1 is essential in the embryo proper. Loss of LRP1 leads to lethal vascular defects with lack of proper investment with mural cells of both large and small vessels. We further demonstrate that LRP1 modulates Gi-dependent sphingosine-1-phosphate (S1P) signaling and integrates S1P and PDGF-BB signaling pathways, which are both crucial for mural cell recruitment, via its intracellular domain. Loss of LRP1 leads to a lack of S1P-dependent inhibition of RAC1 and loss of constraint of PDGF-BB-induced cell migra…

AngiogenesisBlotting WesternBecaplerminEmbryonic DevelopmentNeovascularization PhysiologicRAC1BiologyReal-Time Polymerase Chain ReactionMural cellchemistry.chemical_compoundMiceCell MovementSphingosineHuman Umbilical Vein Endothelial CellsAnimalsHumansSphingosine-1-phosphateMolecular BiologyResearch ArticlesIn Situ HybridizationSphingosineTumor Suppressor ProteinsCell migrationCell BiologyProto-Oncogene Proteins c-sisLRP1ImmunohistochemistryCell biologyMicroscopy ElectronchemistryReceptors LDLLow-density lipoproteinSignal transductionLysophospholipidsGenetic EngineeringLow Density Lipoprotein Receptor-Related Protein-1Developmental BiologySignal Transduction
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An active form of sphingosine kinase-1 is released in the extracellular medium as component of membrane vesicles shed by two human tumor cell line.

2010

Expression of sphingosine kinase-1 (SphK-1) correlates with a poor survival rate of tumor patients. This effect is probably due to the ability of SphK-1 to be released into the extracellular medium where it catalyzes the biosynthesis of sphingosine-1-phosphate (S1P), a signaling molecule endowed with profound proangiogenic effects. SphK-1 is a leaderless protein which is secreted by an unconventional mechanism. In this paper, we will show that in human hepatocarcinoma Sk-Hep1 cells, extracellular signaling is followed by targeting the enzyme to the cell surface and parallels targeting of FGF-2 to the budding vesicles. We will also show that SphK-1 is present in a catalitycally active form i…

Article SubjectNeutral CeramidasebiologySphingosineVesicleCellmembrane vesicleslcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogensSphK vesicleslcsh:RC254-282Cell biologychemistry.chemical_compoundmedicine.anatomical_structureOncologySphingosine kinase 1chemistryBiosynthesisCell cultureSettore BIO/10 - Biochimicabiology.proteinExtracellularmedicinesphingosine kinase; ceramidase; tumoe cells. microvesiclesResearch Article
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Glucosylsphingosine (Lyso-Gb1) as a reliable biomarker in Gaucher disease: a narrative review

2023

Abstract Background Gaucher disease (GD) is a rare, inherited, autosomal recessive disorder caused by a deficiency of the lysosomal enzyme, acid β-glucosidase. Its diagnosis is achieved via measurements of acid β-glucosidase activity in either fresh peripheral blood leukocytes or dried blood spots, and confirmed by identifying characteristic mutations in the GBA1 gene. Currently, several biomarkers are available for disease monitoring. Chitotriosidase has been used over the last 20 years to assess the severity of GD, but lacks specificity in GD patients. Conversely, the deacylated form of glucosylceramide, glucosylsphingosine (also known as lyso-Gb1), represents a more reliable biomarker ch…

Biomarker Gaucher disease Glucosylsphingosine Lyso-Gb1Pharmacology (medical)General MedicineGenetics (clinical)
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H7, a protein kinase C inhibitor, increases the glutathione content of neuroblastoma cells

1992

AbstractIt is shown that the intracellular glutathione (GSH) concentration of neuroblastoma-2a cells in culture increases with a maximum at 24 h after starting treatment with 1-(5-isoquinolinylsulfonyl)-2-methylpiperazine (H7), an inhibitor of protein kinase C (PKC). Other inhibitors of this and other protein kinases, e.g. sphingosine, staurosporine, and HA 1004, at the concentrations tested, had a less marked or negligible effect on intracellular GSH concentration. 12-O-Tetradecanoylphorbol-13-acetate (TPA) was also tested and showed no significant effect 24 h after addition.

BiophysicsBiologyBiochemistryPiperazinesCellular differentiationchemistry.chemical_compoundMiceNeuroblastomaAlkaloidsStructural BiologySphingosineProtein kinase C1-(5-Isoquinolinesulfonyl)-2-MethylpiperazineGeneticsmedicineTumor Cells CulturedStaurosporineAnimalsNeuroblastoma cellMolecular BiologyProtein kinase CSulfonamidesSphingosineKinaseCell BiologyGlutathioneIsoquinolinesStaurosporineMolecular biologyGlutathioneEnzyme ActivationBiochemistrychemistryEnzyme inhibitor1-(5-Isoquinolinylsulfonyl)-2-methylpiperazine1-(5-Isoquinolinesulfonyl)-2-Methylpiperazinebiology.proteinH7Intracellularmedicine.drugFEBS Letters
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A sphingosine kinase inhibitor combined with temozolomide induces glioblastoma cell death through accumulation of dihydrosphingosine and dihydroceram…

2014

AbstractGlioblastomas (GBMs) are very aggressive tumors with low chemosensitivity. The DNA-alkylating agent temozolomide (TMZ) is currently the most efficient chemotoxic drug for GBM therapy; however, many patients develop resistance to TMZ. Combining TMZ with another agent could present an improved treatment option if it could overcome TMZ resistance and avoid side effects. Sphingosine kinase inhibitors (SKIs) have emerged as anticancer agents. Sphingosine kinases are often overexpressed in tumors where their activity of phosphorylating sphingosine (Sph) contributes to tumor growth and migration. They control the levels of the pro-apoptotic ceramide (Cer) and Sph and of the pro-survival sp…

Cancer ResearchCeramideProgrammed cell deathImmunologySphingosine kinaseAntineoplastic AgentsApoptosisBiologyCeramidesCellular and Molecular Neurosciencechemistry.chemical_compoundSphingosineCell Line TumorAutophagyTemozolomideHumansEnzyme InhibitorsCytotoxicitySphingosineCell DeathKinaseBrain NeoplasmsAutophagyCell BiologyEndoplasmic Reticulum StressCell biologyDacarbazinePhosphotransferases (Alcohol Group Acceptor)chemistryApoptosisDrug Resistance NeoplasmCancer researchDrug Therapy CombinationOriginal ArticleGlioblastomaCell deathdisease
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Cardioprotection by gene therapy

2015

Ischemic heart disease remains the leading cause of death worldwide. Ischemic pre-, post-, and remote conditionings trigger endogenous cardioprotection that renders the heart resistant to ischemic-reperfusion injury (IRI). Mimicking endogenous cardioprotection by modulating genes involved in cardioprotective signal transduction provides an opportunity to reproduce endogenous cardioprotection with better possibilities of translation into the clinical setting. Genes and signaling pathways by which conditioning maneuvers exert their effects on the heart are partially understood. This is due to the targeted approach that allowed identifying one or a few genes associated with IRI and cardioprote…

Cardioprotectionmedicine.medical_specialtybiologybusiness.industryGene targetingSphingosine kinase 1Heat shock proteinInternal medicineGene expressionmedicinebiology.proteinCardiologyHepatocyte growth factorSignal transductionCardiology and Cardiovascular MedicinebusinessTranscription factormedicine.drugInternational Journal of Cardiology
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Membrane protein oxidation determines neuronal degeneration

2015

Oxidative stress is an early hallmark in neurodegenerative disorders such as Alzheimer's and Parkinson's diseases. However, the critical biochemical effector mechanisms of oxidative neurotoxicity have remained surprisingly elusive. In screening various peroxides and potential substrates of oxidation for their effect on neuronal survival, we observed that intramembrane compounds were significantly more active than aqueous or amphiphilic compounds. To better understand this result, we synthesized a series of competitive and site-specific membrane protein oxidation inhibitors termed aminoacyllipids, whose structures were designed on the basis of amino acids frequently found at the protein-lipi…

Cell SurvivalBiologyProtein oxidationmedicine.disease_causeBiochemistryProtein Structure SecondaryRats Sprague-DawleyCellular and Molecular Neurosciencechemistry.chemical_compoundmedicineAnimalsLipid bilayerCells CulturedNeuronsSphingosineNeurodegenerationNeurotoxicityMembrane Proteinsmedicine.diseaseTransmembrane proteinRatsCell biologyOxidative StressMembrane proteinchemistryNerve DegenerationReactive Oxygen SpeciesOxidation-ReductionOxidative stressJournal of Neurochemistry
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