Search results for " Mitogen-Activated Protein Kinases"

showing 10 items of 175 documents

Time-course of thiol oxidation of protein phosphatases during cerulein-induced acute pancreatitis

2018

Acute pancreatitis (AP) is an acute inflammatory process of the pancreatic gland. The aim of this work was to evaluate the role of thiol oxidation of key proteins that can be involved in the regulation of the inflammatory process during AP. AP was induced in C57BL/6 mice by 7 hourly subcutaneous injections of cerulein (50 ug/kg bw). Animals were sacrificed after 1, 3, 5 and 7 injections of cerulein. One hour after the first injection, hyperoxidation of peroxiredoxin 1–4 was detected coinciding with a H2O2 peak. Three hours later, a marked up-regulation of mRNA and protein expression of sulfiredoxin, partially mediated by Nrf-2, takes place. The up-regulation of sulfiredoxin seems to be resp…

0301 basic medicineMessenger RNA030102 biochemistry & molecular biologyChemistryp38 mitogen-activated protein kinasesThiol oxidationPhosphataseProtein phosphatase 2Pharmacologymedicine.diseaseBiochemistry03 medical and health sciencesSulfiredoxin0302 clinical medicine030220 oncology & carcinogenesisPhysiology (medical)medicineAcute pancreatitisPeroxiredoxinFree Radical Biology and Medicine
researchProduct

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
researchProduct

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
researchProduct

HSP60 activity on human bronchial epithelial cells

2017

HSP60 has been implicated in chronic inflammatory disease pathogenesis, including chronic obstructive pulmonary disease (COPD), but the mechanisms by which this chaperonin would act are poorly understood. A number of studies suggest a role for extracellular HSP60, since it can be secreted from cells and bind Toll-like receptors; however, the effects of this stimulation have never been extensively studied. We investigated the effects (pro- or anti-inflammatory) of HSP60 in human bronchial epithelial cells (16-HBE) alone and in comparison with oxidative, inflammatory, or bacterial challenges. 16-HBE cells were cultured for 1–4 h in the absence or presence of HSP60, H2O2, lipopolysaccharide (…

0301 basic medicinep38αSettore BIO/17 - IstologiaLipopolysaccharidep38 mitogen-activated protein kinasesImmunologyStimulationBronchip38 Mitogen-Activated Protein KinasesERK1Cell LinePathogenesisMitochondrial Proteins03 medical and health scienceschemistry.chemical_compound0302 clinical medicineOriginal Research ArticlesHumansImmunology and AllergyCOPDInterleukin 8Protein kinase AReceptor16-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; TLR-4; p38αPharmacologyIL-8Settore BIO/16 - Anatomia UmanaInterleukin-8JNK1NF-κB p65 subunitEpithelial CellsTLR-4Chaperonin 60MyD88Interleukin-1016-HBEToll-Like Receptor 416-HBE; COPD; CREB1; ERK1; HSP60; IL-10; IL-8; JNK1; MyD88; NF-κB p65 subunit; p38α; TLR-4; Immunology and Allergy; Immunology; PharmacologyInterleukin 10030104 developmental biologychemistry030220 oncology & carcinogenesisIL-10Cancer researchCREB1NF-κB p65 subunitHSP60p38α
researchProduct

Wip1 phosphatase: between p53 and MAPK kinases pathways.

2016

IF 5.008; International audience; Cells undergoing oncogenic transformation frequently inactivate tumor suppressor pathways that could prevent their uncontrolled growth. Among those pathways p53 and p38MAPK pathways play a critical role in regulation of cell cycle, senescence and cell death in response to activation of oncogenes, stress and DNA damage. Consequently, these two pathways are important in determining the sensitivity of tumor cells to anti-cancer treatment. Wild type p53-induced phosphatase, Wip1, is involved in governance of both pathways. Recently, strategies directed to manipulation with Wip1 activity proposed to advance current day anticancer treatment and novel chemical com…

0301 basic medicinep53Programmed cell deathDNA damagetumor suppressorPhosphatase[SDV.CAN]Life Sciences [q-bio]/Cancer[SDV.BC]Life Sciences [q-bio]/Cellular BiologyReviewPyruvate dehydrogenase phosphataseBiologyBioinformaticsmedicine.disease_causechemotherapyp38 Mitogen-Activated Protein Kinases[ SDV.CAN ] Life Sciences [q-bio]/Cancerphosphatase03 medical and health sciencesmedicineAnimalsHumansGenetically modified animal[ SDV.BC ] Life Sciences [q-bio]/Cellular BiologyCell CycleCell cycleCell biologyProtein Phosphatase 2C030104 developmental biologyCell Transformation NeoplasticOncologyMutationSignal transductionTumor Suppressor Protein p53CarcinogenesisDNA DamageSignal TransductionOncotarget
researchProduct

Multifaceted Mechanisms of WY-14643 to Stabilize the Blood-Brain Barrier in a Model of Traumatic Brain Injury

2017

The blood-brain barrier (BBB) is damaged during ischemic insults such as traumatic brain injury or stroke. This contributes to vasogenic edema formation and deteriorate disease outcomes. Enormous efforts are pursued to understand underlying mechanisms of ischemic insults and develop novel therapeutic strategies. In the present study the effects of PPARα agonist WY-14643 were investigated to prevent BBB breakdown and reduce edema formation. WY-14643 inhibited barrier damage in a mouse BBB in vitro model of traumatic brain injury based on oxygen/glucose deprivation in a concentration dependent manner. This was linked to changes of the localization of tight junction proteins. Furthermore, WY-1…

0301 basic medicinepirinixic acidTraumatic brain injuryp38 mitogen-activated protein kinasesIschemiaischemiaPharmacologyBlood–brain barrierPPARαlcsh:RC321-57103 medical and health sciencesCellular and Molecular Neuroscience0302 clinical medicineDownregulation and upregulationmedicinelcsh:Neurosciences. Biological psychiatry. NeuropsychiatryMolecular BiologyOriginal ResearchTight junctionbusiness.industryKinasetraumatic brain injuryblood-brain barriermedicine.diseasestroke030104 developmental biologymedicine.anatomical_structureKnockout mousebusinessNeuroscience030217 neurology & neurosurgeryNeuroscienceFrontiers in Molecular Neuroscience
researchProduct

Posttranslationally modified proteins as mediators of sustained intestinal inflammation.

2006

Oxidative and carbonyl stress leads to generation of N(epsilon)-carboxymethyllysine-modified proteins (CML-mps), which are known to bind the receptor for advanced glycation end products (RAGE) and induce nuclear factor (NF)-kappaB-dependent proinflammatory gene expression. To determine the impact of CML-mps in vivo, RAGE-dependent sustained NF-kappaB activation was studied in resection gut specimens from patients with inflammatory bowel disease. Inflamed gut biopsy tissue demonstrated a significant up-regulation of RAGE and increased NF-kappaB activation. Protein extracts from the inflamed zones, but not from noninflamed resection borders, caused perpetuated NF-kappaB activation in cultured…

AdultCell ExtractsMaleReceptor for Advanced Glycation End ProductsInflammationBiologyInflammatory bowel diseasep38 Mitogen-Activated Protein KinasesPathology and Forensic MedicineProinflammatory cytokineRAGE (receptor)MiceGlycationhemic and lymphatic diseasesGene expressionmedicineAnimalsCalgranulin BHumansCalgranulin AIntestinal MucosaReceptors ImmunologicReceptorProtein Kinase InhibitorsMice KnockoutMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3LysineNF-kappa Bnutritional and metabolic diseasesEndothelial Cellsmedicine.diseaseNFKB1Inflammatory Bowel DiseasesIntestinesDisease Models AnimalImmunologyCancer researchFemalemedicine.symptomProtein Processing Post-TranslationalRegular ArticlesThe American journal of pathology
researchProduct

Repeated muscle biopsies through a single skin incision do not elicit muscle signaling, but IL-6 mRNA and STAT3 phosphorylation increase in injured m…

2011

To determine if muscle biopsies can be repeated using a single small (5–6 mm) skin incision without inducing immediate MAPK activation or inflammation in the noninjured areas, the phosphorylation of ERK1/2, p38-MAPK, c-Jun NH2-terminal kinases (JNKs), IκBα, IKKα, and signal transducer and activator of transcription 3 (STAT3) was examined concurrent with IL-6 mRNA in six muscle biopsies obtained from the vastus lateralis of five men. Four biopsies were obtained through the same incision (5–6 mm) from the right leg (taken at 0, 30, 123, and 126 min) and another two each from new incisions performed in the left leg (at 31 and 120 min), while the subjects rested supine. The first three biopsie…

AdultMaleSTAT3 Transcription FactorMAPK/ERK pathwaymedicine.medical_specialtyPathologyTime FactorsPhysiologyBiopsyInflammationp38 Mitogen-Activated Protein KinasesQuadriceps MuscleMuscular DiseasesNF-KappaB Inhibitor alphaPhysiology (medical)Internal medicinemedicineHumansRNA MessengerPhosphorylationSTAT3Interleukin 6Mitogen-Activated Protein Kinase 1Analysis of VarianceWound HealingMitogen-Activated Protein Kinase 3Skin incisionbiologyInterleukin-6JNK Mitogen-Activated Protein KinasesIl 6 mrnaI-kappa B KinaseUp-RegulationEndocrinologybiology.proteinSTAT proteinPhosphorylationI-kappa B Proteinsmedicine.symptomSignal TransductionJournal of Applied Physiology
researchProduct

Vitamin C and E supplementation alters protein signalling after a strength training session, but not muscle growth during 10 weeks of training

2014

This study investigated the effects of vitamin C and E supplementation on acute responses and adaptations to strength training. Thirty-two recreationally strength-trained men and women were randomly allocated to receive a vitamin C and E supplement (1000 mg day(-1) and 235 mg day(-1), respectively), or a placebo, for 10 weeks. During this period the participants' training involved heavy-load resistance exercise four times per week. Muscle biopsies from m. vastus lateralis were collected, and 1 repetition maximum (1RM) and maximal isometric voluntary contraction force, body composition (dual-energy X-ray absorptiometry), and muscle cross-sectional area (magnetic resonance imaging) were measu…

AdultMalemedicine.medical_specialtyJournal ClubPhysiologyStrength trainingMAP Kinase Signaling Systemmedicine.medical_treatmentMolecular and CellularMuscle ProteinsIsometric exerciseAscorbic AcidBiologyp38 Mitogen-Activated Protein KinasesMuscle hypertrophyIsometric ContractionInternal medicinemedicineHumansVitamin Eta315Leg pressMuscle SkeletalMitogen-Activated Protein Kinase 1Mitogen-Activated Protein Kinase 3Vitamin Cta1184Vitamin EBiceps curlRibosomal Protein S6 Kinases 70-kDaResistance TrainingVitaminsAscorbic acidAdaptation PhysiologicalEndocrinologyDietary SupplementsFemale
researchProduct

Regulation of the effects of CYP2E1-induced oxidative stress by JNK signaling

2014

The generation of excessive amounts of reactive oxygen species (ROS) leads to cellular oxidative stress that underlies a variety of forms of hepatocyte injury and death including that from alcohol. Although ROS can induce cell damage through direct effects on cellular macromolecules, the injurious effects of ROS are mediated largely through changes in signal transduction pathways such as the mitogen-activated protein kinase c-Jun N-terminal kinase (JNK). In response to alcohol, hepatocytes have increased levels of the enzyme cytochrome P450 2E1 (CYP2E1) which generates an oxidant stress that promotes the development of alcoholic steatosis and liver injury. These effects are mediated in larg…

Alcoholic liver diseaseClinical BiochemistryReview ArticleMitogen-activated protein kinase kinasemedicine.disease_causeBiochemistryCytochrome P450 2E10302 clinical medicineMolecular Targeted TherapyMitogen-activated protein kinaseslcsh:QH301-705.5c-Jun N-terminal kinasechemistry.chemical_classificationTNF tumor necrosis factorlcsh:R5-9200303 health sciencesCell DeathCYP2E1 cytochrome P450 2E1Cytochrome P-450 CYP2E13. Good healthCell biologyPKD protein kinase DLiverJNK c-Jun N-terminal kinaseSab SH3 homology associated BTK binding protein030211 gastroenterology & hepatologySignal transductionlcsh:Medicine (General)MAP Kinase Signaling SystemAPAP acetaminophenMKK MAPK kinaseBiology03 medical and health sciencesROS reactive oxygen speciesPKC protein kinase CmedicineAnimalsHumansMAPKKK MAPK kinase kinaseProtein kinase ACell damage030304 developmental biologyReactive oxygen speciesMAP kinase kinase kinaseOrganic ChemistryJNK Mitogen-Activated Protein KinasesAlcoholic liver diseasemedicine.diseaseERK1/2 extracellular signal-regulated kinase 1/2Fatty Liverlcsh:Biology (General)chemistryOxidative stressNAFLD nonalcoholic fatty liver diseaseReactive Oxygen SpeciesMAPK mitogen-activated protein kinaseOxidative stressRedox Biology
researchProduct