Search results for "c-Mer Tyrosine Kinase"

showing 5 items of 5 documents

Palmitoylethanolamide Promotes a Proresolving Macrophage Phenotype and Attenuates Atherosclerotic Plaque Formation

2018

Objective— Palmitoylethanolamide is an endogenous fatty acid mediator that is synthetized from membrane phospholipids by N -acyl phosphatidylethanolamine phospholipase D. Its biological actions are primarily mediated by PPAR-α (peroxisome proliferator-activated receptors α) and the orphan receptor GPR55. Palmitoylethanolamide exerts potent anti-inflammatory actions but its physiological role and promise as a therapeutic agent in chronic arterial inflammation, such as atherosclerosis remain unexplored. Approach and Results— First, the polarization of mouse primary macrophages towards a proinflammatory phenotype was found to reduce N -acyl phosphatidylethanolamine phospholipase D expression …

0301 basic medicineCannabinoid receptorTime FactorsMice Knockout ApoECHOLESTEROL TRANSPORTAnti-Inflammatory AgentsPhospholipaseProto-Oncogene Maschemistry.chemical_compoundCannabinoid receptor type 2Receptors CannabinoidAortachemistry.chemical_classificationMARROW-DERIVED CELLSAPOPTOTIC CELL ACCUMULATIONPlaque AtheroscleroticCell biologymacrophagesDENSITY-LIPOPROTEIN RECEPTORPhenotypeREDUCES INFLAMMATIONCB2 RECEPTOREthanolaminesFemaleCardiology and Cardiovascular MedicineSCAVENGER RECEPTORAortic DiseasesPalmitic Acidsta3111fatty acidsCell Line03 medical and health sciencesMediatorPhagocytosisPhospholipase DAnimalsHumansScavenger receptorCANNABINOID RECEPTORPhosphatidylethanolaminePalmitoylethanolamidec-Mer Tyrosine KinaseFatty acidcholesterolta3121AmidesRatsMice Inbred C57BLDisease Models Animal030104 developmental biologychemistryinflammationRECEPTOR CLASS-BatherosclerosisCONTACT ALLERGIC DERMATITISArteriosclerosis Thrombosis and Vascular Biology
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MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis

2017

Atherothrombotic vascular disease is often triggered by a distinct type of atherosclerotic lesion that displays features of impaired inflammation resolution, notably a necrotic core and thinning of a protective fibrous cap that overlies the core. A key cause of plaque necrosis is defective clearance of apoptotic cells, or efferocytosis, by lesional macrophages, but the mechanisms underlying defective efferocytosis and its possible links to impaired resolution in atherosclerosis are incompletely understood. Here, we provide evidence that proteolytic cleavage of the macrophage efferocytosis receptor c-Mer tyrosine kinase (MerTK) reduces efferocytosis and promotes plaque necrosis and defective…

0301 basic medicineCarotid Artery DiseasesMalePathologymedicine.medical_specialtyNecrosisCardiology030204 cardiovascular system & hematologyBiologyC-Mer Tyrosine KinaseProinflammatory cytokine03 medical and health sciencesMiceNecrosis0302 clinical medicineProto-Oncogene ProteinsmedicineAnimalsHumansEfferocytosisMice Knockoutc-Mer Tyrosine KinaseBrief ReportFibrous capReceptor Protein-Tyrosine KinasesGeneral MedicineMERTKPlaque Atherosclerotic030104 developmental biologymedicine.anatomical_structureReceptors LDLApoptosisProteolysisFemalemedicine.symptomTyrosine kinase
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CAMKIIγ suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis

2017

Atherosclerosis is the underlying etiology of cardiovascular disease, the leading cause of death worldwide. Atherosclerosis is a heterogeneous disease in which only a small fraction of lesions lead to heart attack, stroke, or sudden cardiac death. A distinct type of plaque containing large necrotic cores with thin fibrous caps often precipitates these acute events. Here, we show that Ca2+/calmodulin-dependent protein kinase gamma (CaMKII gamma) in macrophages plays a major role in the development of necrotic, thin-capped plaques. Macrophages in necrotic and symptomatic atherosclerotic plaques in humans as well as advanced atherosclerotic lesions in mice demonstrated activation of CaMKII. We…

0301 basic medicineMalePathologymedicine.medical_specialtyPhagocytosisGene ExpressionInflammationApoptosisMice TransgenicBiologyPHAGOCYTOSISLIPID MEDIATORS03 medical and health sciencesNecrosisENDOPLASMIC-RETICULUM STRESSINFLAMMATIONCa2+/calmodulin-dependent protein kinaseC/EBP HOMOLOGOUS PROTEINmedicineMacrophageAnimalsHumansKINASE-IILiver X receptorEfferocytosisCells CulturedLiver X ReceptorsAPOE-DEFICIENT MICEc-Mer Tyrosine KinaseATF6MacrophagesAPOPTOTIC CELL ACCUMULATIONGeneral MedicineMERTKAtherosclerosisPlaque AtheroscleroticActivating Transcription Factor 6Enzyme ActivationMice Inbred C57BL030104 developmental biologyRESOLUTIONmedicine.symptomCalcium-Calmodulin-Dependent Protein Kinase Type 2LIVER-X-RECEPTORResearch ArticleSignal TransductionJournal of Clinical Investigation
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MERTK rs4374383 polymorphism affects the severity of fibrosis in non-alcoholic fatty liver disease

2015

Background & Aim Homozygosity for a common non-coding rs4374383 G>A polymorphism in MERTK (myeloid-epithelial-reproductive tyrosine kinase) has been associated with the protection against fibrosis progression in chronic hepatitis C. The main study objective was to assess whether MERTK AA genotype influences liver fibrosis, and secondarily MERTK expression in patients with non-alcoholic fatty liver disease (NAFLD). We also investigated whether MERTK is expressed in human hepatic stellate cells (HSC) and in murine models of fibrogenesis. Methods We considered 533 consecutive patients who underwent liver biopsy for suspected non-alcoholic steatohepatitis (NASH) without severe obesity from two …

Liver CirrhosisMale0301 basic medicineMessengerMice0302 clinical medicineNon-alcoholic Fatty Liver DiseaseFibrosisInbred BALB CCells CulturedMice Inbred BALB CCulturedmedicine.diagnostic_testMedicine (all)Fatty liverNASHMiddle AgedLiver biopsyFemale030211 gastroenterology & hepatologyAdultmedicine.medical_specialtyMERTKCellsBiology03 medical and health sciencesGeneticProto-Oncogene ProteinsInternal medicinemedicineAnimalsHumansFibrosis; MERTK; NASH; Adult; Animals; Cells Cultured; Female; Humans; Liver Cirrhosis; Male; Mice Inbred BALB C; Middle Aged; Non-alcoholic Fatty Liver Disease; Proto-Oncogene Proteins; RNA Messenger; Receptor Protein-Tyrosine Kinases; Polymorphism Genetic; Medicine (all); HepatologyRNA MessengerPolymorphismPolymorphism Geneticc-Mer Tyrosine KinaseHepatologyGAS6Receptor Protein-Tyrosine Kinasesnafld fibrosis mertkMERTKHepatologymedicine.diseaseFibrosis030104 developmental biologyImmunologyHepatic stellate cellRNASteatohepatitisJournal of Hepatology
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Mer Tyrosine Kinase (MERTK) modulates liver fibrosis progression and hepatocellular carcinoma development.

2022

BackgroundMerTK is a tyrosine kinase receptor that belongs to the TAM (Tyro3/Axl/Mer) receptor family. It is involved in different processes including cellular proliferation/survival, cellular adhesion/migration, and release of the inflammatory/anti-inflammatory cytokines. Although it is reported that MERTK polymorphisms affect the severity of viral and metabolic liver diseases, being able to influence fibrosis progression and hepatocellular carcinoma development, the mechanisms remain unknown. Methods: using a microarray approach, we evaluated the liver expression of genes involved in fibrogenesis and hepatocarcinogenesis in patient with chronic hepatitis C (CHC), stratified for MERTK geno…

Liver CirrhosisSettore MED/12 - GastroenterologiaCarcinoma Hepatocellularc-Mer Tyrosine KinaseMer Tyrosine Kinase polymorphism (MERTK polymorphism) WNT gene family pathway (WNT pathway) hepatocellular carcinoma liver fibrosis matrix metallopeptidase Metalloproteases Protein-Tyrosine Kinases Liver CirrhosisImmunologyLiver NeoplasmsProtein-Tyrosine KinasesFibrosisSettore BIO/13 - Biologia ApplicataProto-Oncogene ProteinsMetalloproteasesImmunology and AllergyHumansFrontiers in immunology
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