Search results for "CD3"

showing 10 items of 420 documents

Dexamethasone Inhibits the Pro-Angiogenic Potential of Primary Human Myoblasts

2021

Tissue regeneration depends on the complex processes of angiogenesis, inflammation and wound healing. Regarding muscle tissue, glucocorticoids (GCs) inhibit pro-inflammatory signalling and angiogenesis and lead to muscle atrophy. Our hypothesis is that the synthetic GC dexamethasone (dex) impairs angiogenesis leading to muscle atrophy or inhibited muscle regeneration. Therefore, this study aims to elucidate the effect of dexamethasone on HUVECs under different conditions in mono- and co-culture with myoblasts to evaluate growth behavior and dex impact with regard to muscle atrophy and muscle regeneration. Viability assays, qPCR, immunofluorescence as well as ELISAs were performed on HUVECs,…

Vascular Endothelial Growth Factor A0301 basic medicineMuscle tissueCD31endocrine systemQH301-705.5AngiogenesisMyoblasts SkeletalNeovascularization PhysiologicInflammationdexamethasonehuman primary myoblastsArticleCatalysisInorganic Chemistry03 medical and health sciences0302 clinical medicineHuman Umbilical Vein Endothelial Cellsmedicinepolycyclic compoundsHumansMyocyteBiology (General)Physical and Theoretical ChemistryQD1-999Molecular BiologySpectroscopyHUVECsTube formationChemistryOrganic ChemistryGeneral Medicineco-cultureVEGFCoculture TechniquesMuscle atrophyComputer Science ApplicationsCell biologyChemistry030104 developmental biologymedicine.anatomical_structureGene Expression RegulationCD31medicine.symptomWound healing030217 neurology & neurosurgeryhormones hormone substitutes and hormone antagonistsInternational Journal of Molecular Sciences
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Human Fetal Aorta Contains Vascular Progenitor Cells Capable of Inducing Vasculogenesis, Angiogenesis, and Myogenesis in Vitro and in a Murine Model …

2007

Vasculogenesis, the formation of blood vessels in embryonic or fetal tissue mediated by immature vascular cells (ie, angioblasts), is poorly understood. We report the identification of a population of vascular progenitor cells (hVPCs) in the human fetal aorta composed of undifferentiated mesenchymal cells that coexpress endothelial and myogenic markers. Under culture conditions that promoted cell differentiation, hVPCs gave rise to a mixed population of mature endothelial and mural cells when progenitor cells were stimulated with vascular endothelial growth factor-A or platelet-derived growth factor-betabeta. hVPCs grew as nonadherent cells and, when embedded in a three-dimensional collagen…

Vascular Endothelial Growth Factor AAngiogenesisBecaplerminNeovascularization PhysiologicAntigens CD34BiologyMuscle DevelopmentMural cellPathology and Forensic MedicineAngiopoietin-2MiceFetusVasculogenesisAntigens CDIschemiaAnimalsHumansCell LineageAC133 AntigenProgenitor cellAortaCells CulturedGlycoproteinsPlatelet-Derived Growth FactorStem CellsProto-Oncogene Proteins c-sisVascular Endothelial Growth Factor Receptor-2Cell biologyEndothelial stem cellVascular endothelial growth factor BVascular endothelial growth factor AVascular endothelial growth factor CImmunologyBlood VesselsPeptidesBiomarkersRegular ArticlesThe American Journal of Pathology
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Heart infarct in NOD-SCID mice: therapeutic vasculogenesis by transplantation of human CD34+ cells and low dose CD34+KDR+ cells

2004

Hematopoietic (Hem) and endothelial (End) lineages derive from a common progenitor cell, the hemangioblast: specifically, the human cord blood (CB) CD34+KDR+ cell fraction comprises primitive Hem and End cells, as well as hemangioblasts. In humans, the potential therapeutic role of Hem and End progenitors in ischemic heart disease is subject to intense investigation. Particularly, the contribution of these cells to angiogenesis and cardiomyogenesis in myocardial ischemia is not well established. In our studies, we induced myocardial infarct (MI) in the immunocompromised NOD-SCID mouse model, and monitored the effects of myocardial transplantation of human CB CD34+ cells on cardiac function.…

Vascular Endothelial Growth Factor AneoangiogenesisTime FactorsAngiogenesisCell TransplantationHeart VentriclesCD34Myocardial InfarctionAntigens CD34ApoptosisMice SCIDBiologySCIDPeripheral blood mononuclear cellBiochemistryCulture Media Serum-FreeSerum-FreeCell FusionMiceVasculogenesisMice Inbred NODparasitic diseasesGeneticsAnimalsHumansVentricular Functionendothelial precursorsCell LineageProgenitor cellAntigensMolecular Biologyneoangiogenesis endothelial precursors hematopoietic stem cellsHemodynamicsFetal BloodVascular Endothelial Growth Factor Receptor-2Coculture Techniqueshematopoietic stem cellsCulture MediaTransplantationAutocrine CommunicationCord bloodImmunologycardiovascular systemCancer researchHemangioblastInbred NODCD34neoangiogenesis; endothelial precursors; hematopoietic stem cells; Animals; Antigens CD34; Apoptosis; Autocrine Communication; Cell Fusion; Cell Lineage; Coculture Techniques; Culture Media Serum-Free; Fetal Blood; Heart Ventricles; Hemodynamics; Humans; Mice; Mice Inbred NOD; Mice SCID; Myocardial Infarction; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Ventricular Function; Cell Transplantation; Biotechnology; Biochemistry; Molecular Biology; GeneticsBiotechnology
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HSP27: A Therapeutic Target in Myelofibrosis

2016

Abstract Myelofibrosis (MF) is the most aggressive myeloproliferative neoplasms (MPN) with the highest degree of morbidity and mortality, including progressive bone marrow fibrosis resulting into bone marrow failure. JAK2 kinase inhibitors have been successfully used for a few years in MPN and more particularly for MF treatment. Despite their beneficial effects on spleen size and symptoms, JAK2 inhibitors induce low molecular and survival responses underscoring the urgent need for other therapeutic approaches. Recently, heat shock protein 90 (HSP90) - known to stabilize JAK2 - has been reported as a promising therapeutic target in MPN. However HSP90 inhibitors show toxicity and induce the e…

White pulpImmunologyCD34Bone marrow failureCell BiologyHematologyBiologymedicine.diseaseBiochemistry03 medical and health sciencesLeukemia0302 clinical medicinemedicine.anatomical_structureMegakaryocyteFibrosis030220 oncology & carcinogenesisImmunologymedicineBone marrowMyelofibrosis030215 immunologyBlood
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Depletion ofL-arginine induces autophagy as a cytoprotective response to endoplasmic reticulum stress in human T lymphocytes

2012

PMCID: PMC3494587

X-Box Binding Protein 1Proteasome Endopeptidase ComplexProgrammed cell deathXBP1CD3 ComplexMAP Kinase Signaling SystemRNA SplicingT-LymphocytesT cellDown-RegulationApoptosisRegulatory Factor X Transcription FactorsUbiquitin-Activating EnzymesProtein Serine-Threonine KinasesBiologyArginineLymphocyte ActivationAutophagy-Related Protein 7Jurkat cellsJurkat CellsEndoribonucleasesAutophagymedicineHumansMolecular BiologyCell ProliferationTOR Serine-Threonine KinasesAutophagyMembrane ProteinsCell BiologyBECN1Endoplasmic Reticulum StressG1 Phase Cell Cycle CheckpointsBasic Research Paper3. Good healthCell biologyDNA-Binding Proteinsmedicine.anatomical_structureCytoprotectionApoptosisUnfolded protein responseBeclin-1MitogensApoptosis Regulatory ProteinsLysosomesProto-Oncogene Proteins c-aktTranscription FactorsAutophagy
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Do we taste fat?

2006

Sense of taste informs the body about the quality of ingested foods. Five sub-modalities allowing the perception of sweet, salty, sour, bitter, and umami stimuli are classically depicted. However, the inborn attraction of mammals for fatty foods raises the possibility of an additional oro-sensory modality devoted to fat perception. During a long time, dietary lipids were thought to be detected only by trigeminal (texture perception), retronasal olfactory, and post-ingestive cues. This minireview analyses recent findings showing that the gustation also plays a significant role in dietary lipid perception.

[SCCO.NEUR] Cognitive science/NeuroscienceCD36gustationLipidsCD36.
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Détection orosensorielle des lipides alimentaires chez la souris : mécanismes impliqués et altérations au cours de l'obésité

2015

Dietary lipids are detected by the gustatory system in rodents and humans. Two candidate lipid-receptors are found in taste buds: CD36, which is involved in the fat taste as shown by studies conducted in our laboratory, and GPR120. Our results show that GPR120 is not directly involved in the gustatory detection of lipids in mice, but could rather be involved in the modulation of the sensitivity for fat. When this gustatory system works properly, food choices can meet the organism’s energy needs. Besides, the pleasure brought by the consumption of palatable foods is satisfied. However, obese people often overconsume energy-dense food. In the central nervous system, perturbations of the rewar…

[SDV.MHEP.EM] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismInflammationSantéMicrobioteLPSGoût du grasGPR120Food behaviorMicrobiota[ SDV.AEN ] Life Sciences [q-bio]/Food and NutritionLipides[SDV.MHEP.EM]Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolism[ SDV.MHEP.EM ] Life Sciences [q-bio]/Human health and pathology/Endocrinology and metabolismLipids[SDV.AEN] Life Sciences [q-bio]/Food and NutritionComportement alimentaireHealthObesityObésitéCD36[SDV.AEN]Life Sciences [q-bio]/Food and NutritionFat taste
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Role of intestinal epithelial CD36 in obesity and endotoxemia driven by lipid absorption

2021

Intestinal dysbiosis, increased permeability and inflammation are the hallmarks in obese patients, highlighting the role of small intestine beyond providing with calories. CD36 is a ubiquitous scavenger receptor that exhibits high binding affinity for long-chain fatty acids and is highly expressed in enterocytes, endothelial and immune cells. Interestingly, CD36-/- mice and humans with CD36 polymorphisms have an impaired synthesis of triglyceride-rich lipoprotein (TRL). To evaluate the role of CD36 expressed by intestinal-epithelial cells (IEC) in obesity, we conducted experiments on male and female mice deleted in CD36 in IEC (ENT-KO) and control mice (ENT-FL), under standard and high-fat …

[SDV.SA] Life Sciences [q-bio]/Agricultural sciencesLipidesGutObesityObesitéEndotoxémieCd36LipidsIntestinAbsorptionEndotoxemy
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The study of calcium signaling in lipid gustatory cells in mice

2012

The lipid-binding glycoprotein CD36, expressed by circumvallate papillae (CVP) of the mouse tongue, has been shown to be implicated in oro-gustatory perception of dietary lipids. We demonstrate that linoleic acid (LA) by activating sPLA2, cPLA2 and iPLA2 via CD36, produced arachidonic acid (AA) and lyso-phosphatidylcholine (Lyso-PC) which triggered Ca2+ influx in CD36-positive taste bud cells (TBC), purified from mouse CVP. LA induced the production of Ca2+ influx factor (CIF). CIF, AA and Lyso-PC exerted different actions on the opening of store-operated Ca2+ (SOC) channels, constituted of Orai proteins and regulated by STIM1, a sensor of Ca2+ depletion in the endoplasmic reticulum. We use…

[SDV.SA]Life Sciences [q-bio]/Agricultural sciencesLinoleic acidPLA2[SDV.SA] Life Sciences [q-bio]/Agricultural sciencesStim1Préférence gustative lipidiqueSOCAcide linoléiqueCD36[ SDV.SA ] Life Sciences [q-bio]/Agricultural sciencesOro-gustatory lipid preferenceOrai1/3
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Postprandial adaptation of intestinal lipid metabolism : role of CD36 and PPAR beta

2011

Postprandial hypertriglyceridemia is an emerging risk factor for cardiovascular diseases and is associated with metabolic syndrome, obesity and insulin resistance. The small intestine participates in the postprandial triglyceridemia since both the size and number of secreted chylomicrons modulate lipoprotein lipase activity (LPL). Chylomicron synthesis is a complex mechanism in which the lipidation of Apolipoprotein B48 (ApoB48) by the Microsomal Triglyceride Transfer Protein (MTP) and the transfer between reticulum and Golgi in which the Liver Fatty Acid Binding Protein (L -FABP) is involved are limiting steps. An intestinal fat-mediated adaptation in postprandial period has been demonstra…

[SDV.SA]Life Sciences [q-bio]/Agricultural sciences[SDV.SA] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP] Life Sciences [q-bio]/Human health and pathologyTriglycéridémie postprandialedigestive oral and skin physiologyPostprandial triglyceridemiaRécepteurPPAR betaPPAR béta[ SDV.MHEP ] Life Sciences [q-bio]/Human health and pathologyChylomicronslipids (amino acids peptides and proteins)CD36[ SDV.SA ] Life Sciences [q-bio]/Agricultural sciences[SDV.MHEP]Life Sciences [q-bio]/Human health and pathologyReceptor
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