Search results for "PROTEIN KINASE"

showing 10 items of 1188 documents

VEGF-B-induced vascular growth leads to metabolic reprogramming and ischemia resistance in the heart

2014

Abstract Angiogenic growth factors have recently been linked to tissue metabolism. We have used genetic gain‐ and loss‐of function models to elucidate the effects and mechanisms of action of vascular endothelial growth factor‐B (VEGF‐B) in the heart. A cardiomyocyte‐specific VEGF‐B transgene induced an expanded coronary arterial tree and reprogramming of cardiomyocyte metabolism. This was associated with protection against myocardial infarction and preservation of mitochondrial complex I function upon ischemia‐reperfusion. VEGF‐B increased VEGF signals via VEGF receptor‐2 to activate Erk1/2, which resulted in vascular growth. Akt and mTORC1 pathways were upregulated and AMPK downregulated, …

VEGF‐Bmedicine.medical_specialtyMedicine (General)AngiogenesiseducationMOUSE HEARTIschemiaVEGF-B610 Medicine & healthmTORC1ischemiaBiologyQH426-470CONTRIBUTESchemistry.chemical_compoundangiogenesisR5-920CARDIAC-FUNCTIONInternal medicinemedicineGeneticsFAILUREta318Myocardial infarctionFATTY-ACID UPTAKEREPERFUSION INJURY610 Medicine & healthProtein kinase BMYOCARDIAL HYPERTROPHYAMPKta3121medicine.diseaseCell biologyARTERIOGENESISVascular endothelial growth factorMICEEndocrinologychemistry3121 General medicine internal medicine and other clinical medicineendothelial cellMolecular Medicine3111 BiomedicineReperfusion injurymetabolism
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Targeting V-ATPase in primary human monocytes by archazolid potently represses the classical secretion of cytokines due to accumulation at the endopl…

2014

The macrolide archazolid inhibits vacuolar-type H(+)-ATPase (V-ATPase), a proton-translocating enzyme involved in protein transport and pH regulation of cell organelles, and potently suppresses cancer cell growth at low nanomolar concentrations. In view of the growing link between inflammation and cancer, we investigated whether inhibition of V-ATPase by archazolid may affect primary human monocytes that can promote cancer by sustaining inflammation through the release of tumor-promoting cytokines. Human primary monocytes express V-ATPase, and archazolid (10-100nM) increases the vesicular pH in these cells. Archazolid (10nM) markedly reduced the release of pro-inflammatory (TNF-α, interleuk…

Vacuolar Proton-Translocating ATPasesmedicine.medical_specialtyp38 mitogen-activated protein kinasesInflammationBiologyEndoplasmic ReticulumBiochemistryMonocytesCell Linechemistry.chemical_compoundInternal medicinemedicineHumansSecretionPhosphorylationProtein kinase BDNA PrimersPharmacologyBase SequenceDose-Response Relationship DrugReverse Transcriptase Polymerase Chain ReactionEndoplasmic reticulumBafilomycinCell biologyIκBαEndocrinologySecretory proteinMicroscopy FluorescencechemistryCytokinesMacrolidesmedicine.symptomSignal TransductionBiochemical Pharmacology
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Concomitant Use of Statins, Metformin, or Proton Pump Inhibitors in Patients with Advanced Renal Cell Carcinoma Treated with First-Line Combination T…

2022

Background Drug-drug interactions are a major concern in oncology and may potentially affect the outcome of patients with cancer. Objective In this study, we aimed to determine whether the concomitant use of statins, metformin, or proton pump inhibitors affects survival in patients with metastatic renal cell carcinoma treated with first-line combination therapies. Methods Medical records of patients with documented metastatic renal cell carcinoma between January 2016 and November 2021 were reviewed at 17 participating centers. This research was conducted in ten institutions, including both referral centers and local hospitals. Patients were assessed for overall survival, progression-free su…

Vascular Endothelial Growth Factor ACancer ResearchAngiogenesis InhibitorsProton Pump InhibitorsKidney NeoplasmsMetforminTreatment OutcomeOncologyHumansPharmacology (medical)Hydroxymethylglutaryl-CoA Reductase InhibitorsCarcinoma Renal CellProtein Kinase InhibitorsRetrospective StudiesTargeted oncology
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Endothelin-1-Mediated Drug Resistance in EGFR-Mutant Non-Small Cell Lung Carcinoma.

2020

Abstract Progression on therapy in non-small cell lung carcinoma (NSCLC) is often evaluated radiographically, however, image-based evaluation of said therapies may not distinguish disease progression due to intrinsic tumor drug resistance or inefficient tumor penetration of the drugs. Here we report that the inhibition of mutated EGFR promotes the secretion of a potent vasoconstrictor, endothelin-1 (EDN1), which continues to increase as the cells become resistant with a mesenchymal phenotype. As EDN1 and its receptor (EDNR) is linked to cancer progression, EDNR-antagonists have been evaluated in several clinical trials with disappointing results. These trials were based on a hypothesis that…

Vascular Endothelial Growth Factor ACancer ResearchLung NeoplasmsAmbrisentanOncology and CarcinogenesisDrug ResistanceBiological AvailabilityAntineoplastic AgentsDrug resistanceCell LineMiceErlotinib HydrochlorideGefitinibIn vivomedicineAnimalsHumansOncology & CarcinogenesisNon-Small-Cell LungProtein Kinase InhibitorsLungCancerTumor microenvironmentTumorEndothelin-1business.industryCarcinomaLung CancerCancerEvaluation of treatments and therapeutic interventionsGefitinibmedicine.diseaseEndothelin 1Xenograft Model Antitumor AssaysErbB ReceptorsOncologyVasoconstriction5.1 Pharmaceuticals6.1 PharmaceuticalsCancer cellMutationCancer researchNeoplasmDevelopment of treatments and therapeutic interventionsbusinessmedicine.drug
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Glycolytic phenotype and AMP kinase modify the pathologic response of tumor xenografts to VEGF neutralization.

2011

Abstract VEGF antagonists are now widely used cancer therapeutics, but predictive biomarkers of response or toxicity remain unavailable. In this study, we analyzed the effects of anti-VEGF therapy on tumor metabolism and therapeutic response by using an integrated set of imaging techniques, including bioluminescence metabolic imaging, 18-fluorodeoxyglucose positron emission tomography, and MRI imaging and spectroscopy. Our results revealed that anti-VEGF therapy caused a dramatic depletion of glucose and an exhaustion of ATP levels in tumors, although glucose uptake was maintained. These metabolic changes selectively accompanied the presence of large necrotic areas and partial tumor regress…

Vascular Endothelial Growth Factor ACancer Researchmedicine.medical_specialtyMagnetic Resonance SpectroscopyGlucose uptakeBiologyMiceFluorodeoxyglucose F18Internal medicineCell Line TumormedicineAnimalsHumansGlycolysisViability assayProtein kinase AAdenylate KinaseAMPKCancerNeoplasms Experimentalmedicine.diseaseWarburg effectMagnetic Resonance ImagingEndocrinologyPhenotypeOncologyCancer researchTumor necrosis factor alphaGlycolysisCancer research
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Arthrinins A–D: Novel diterpenoids and further constituents from the sponge derived fungus Arthrinium sp.

2011

Bioassay-guided fractionation of a methanolic extract of the fungus Arthrinium sp., isolated from the Mediterranean sponge Geodia cydonium, afforded 10 natural products including five new diterpenoids, arthrinins A-D (1-4) and myrocin D (5). In addition, five known compounds were obtained, which included myrocin A (6), norlichexanthone (7), anomalin A (8), decarboxycitrinone (9) and 2,5-dimethyl-7-hydroxychromone (10). The structures of all isolated compounds were unambiguously elucidated based on extensive 1D and 2D NMR and HR-MS analyzes. The absolute configuration of arthrinins A-D (1-4) was established by the convenient Mosher method performed in NMR tubes and by interpretation of the R…

Vascular Endothelial Growth Factor AClinical BiochemistryPharmaceutical ScienceAntineoplastic AgentsBiochemistryMiceAscomycotaCell Line TumorNeoplasmsDrug DiscoveryAnimalsHumansMTT assayCytotoxicityProtein Kinase InhibitorsMolecular BiologyNeovascularization PathologicKinaseChemistryOrganic ChemistryTerpenoidIn vitroPoriferaEndothelial stem cellVascular endothelial growth factor ABiochemistryCell cultureMolecular MedicineDiterpenesProtein KinasesBioorganic & Medicinal Chemistry
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Reactive oxygen species activation of MAPK pathway results in VEGF upregulation as an undesired irradiation response

2013

Background Radioresistance limits the effectiveness of radiotherapy in head and neck squamous cell carcinoma. We previously demonstrated post-radiogenic mitogen-activated protein kinase (MAPK) pathway activation and vascular endothelial growth factor (VEGF) release resulting in reduced tumor cell response. Here, we examined the association of this mechanism with the induction of reactive oxygen species (ROS) under irradiation (IR). Methods Intracellular ROS after IR were measured. We modeled radiation-induced ROS by exposure of two SCC lines to H2O2 and evaluated the impact of irradiation and ROS on ERK phosphorylation by Western blot, immunohistochemistry, and ELISA. Results We found eleva…

Vascular Endothelial Growth Factor AMAPK/ERK pathwayCancer ResearchPathologymedicine.medical_specialtyMAP Kinase Signaling SystemBlotting WesternEnzyme-Linked Immunosorbent AssayBiologyRadiation TolerancePathology and Forensic Medicinechemistry.chemical_compoundDownregulation and upregulationCell Line TumorNitrilesButadienesmedicineHumansEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesProtein kinase Achemistry.chemical_classificationReactive oxygen speciesHydrogen PeroxideImmunohistochemistryCytoprotectionUp-RegulationVascular endothelial growth factorVascular endothelial growth factor AOtorhinolaryngologychemistryCytoprotectionCarcinoma Squamous CellCancer researchPeriodonticsElectrophoresis Polyacrylamide GelOral SurgeryReactive Oxygen SpeciesIntracellularJournal of Oral Pathology & Medicine
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Activation of mitogen-activated protein kinase extracellular signal-related kinase in head and neck squamous cell carcinomas after irradiation as par…

2010

Background. Irradiation plays a pivotal role in head and neck squamous cell carcinoma (HNSCC) treatment. However, especially recurrent tumors frequently show increased radioresistance. We analyzed irradiation-stimulated mitogen-activated protein kinase (MAPK) signaling pathways to define cellular rescue mechanisms. Methods. Irradiated HNSCC cells were screened for MAPK activation and results were confirmed and refined by functional analyses. Extracellular signal-regulated kinase (ERK) inhibitor U0126 application enabled us to specify postradiogenic cellu- lar responses. Vascular endothelial growth factor (VEGF) levels were analyzed additionally. Results. We observed a pronounced and time-de…

Vascular Endothelial Growth Factor AMAPK/ERK pathwayMAP Kinase Signaling SystemMice NudeMicechemistry.chemical_compoundCell Line TumorRadioresistanceNitrilesButadienesmedicineAnimalsHumansEnzyme InhibitorsExtracellular Signal-Regulated MAP KinasesProtein kinase AbiologyKinasebusiness.industryRadiotherapy Dosagemedicine.diseaseImmunohistochemistryHead and neck squamous-cell carcinomaUp-RegulationVascular endothelial growth factorOtorhinolaryngologychemistryHead and Neck NeoplasmsMitogen-activated protein kinaseCarcinoma Squamous CellCancer researchbiology.proteinMitogen-Activated Protein KinasesSignal transductionbusinessNeoplasm TransplantationSignal TransductionHead & Neck
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Protein kinase C   promotes angiogenic activity of human endothelial cells via induction of vascular endothelial growth factor

2008

Aims Protein kinase C (PKC) plays an important role in the regulation of angiogenesis. However, downstream targets of PKC in endothelial cells are poorly defined. Methods and results mRNA expression of vascular endothelial growth factor (VEGF) was analysed by quantitative real-time RT-PCR in human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells. siRNA was used to knockdown PKC isoforms and VEGF. Matrigel tube formation assay was used to analyse the angiogenic activity of endothelial cells. Phorbol-12-myristate-13-acetate (PMA) enhanced the ability of HUVEC to organize into tubular networks when plated on Matrigel, a phenomenon that could be prevented by PKC inhibi…

Vascular Endothelial Growth Factor Amedicine.medical_specialtyProtein Kinase C-alphaTime FactorsPhysiologyAngiogenesismedicine.medical_treatmentBlotting WesternCarbazolesNeovascularization PhysiologicBiologyPolymerase Chain ReactionCell Linechemistry.chemical_compoundPhysiology (medical)Internal medicinemedicineHumansRNA MessengerRNA Small InterferingCell ShapeProtein Kinase InhibitorsCells CulturedProtein kinase CTube formationMatrigelStem CellsGrowth factorEndothelial CellsUp-RegulationCell biologyEnzyme ActivationEndothelial stem cellVascular endothelial growth factorAutocrine CommunicationVascular endothelial growth factor AReceptors Vascular Endothelial Growth FactorEndocrinologychemistryTetradecanoylphorbol AcetateAngiogenesis Inducing AgentsFibroblast Growth Factor 2RNA InterferenceCardiology and Cardiovascular MedicineCardiovascular Research
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Transmembrane signalling mechanisms regulating expression of cationic amino acid transporters and inducible nitric oxide synthase in rat vascular smo…

1999

The signalling mechanisms involved in the induction of nitric oxide synthase and l-arginine transport were investigated in bacterial lipopolysaccharide (LPS)- and interferon-gamma (IFN-gamma)-stimulated rat cultured aortic smooth muscle cells (RASMCs). The expression profile of transcripts for cationic amino acid transporters (CATs) and their regulation by LPS and IFN-gamma were also examined. Control RASMCs expressed mRNA for CAT-1, CAT-2A and CAT-2B. Levels of all three transcripts were significantly elevated in activated cells. Stimulated CAT mRNA expression and l-arginine transport occurred independently of protein kinase C (PKC), protein tyrosine kinase (PTK) and p44/42 mitogen-activat…

Vascular smooth muscleKinasep38 mitogen-activated protein kinasesCell BiologyBiologyBiochemistryNitric oxideCell biologyNitric oxide synthasechemistry.chemical_compoundchemistrybiology.proteinSignal transductionMolecular BiologyTyrosine kinaseProtein kinase CBiochemical Journal
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